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{{Short description|Process by which neurons communicate with each other by changes in their membrane potentials}}

{{Short description|Process by which neurons communicate with each other by changes in their membrane potentials}}

 

[[File:Action Potential.gif|thumb|upright=1.5|As an action potential (nerve impulse) travels down an [[axon]] there is a change in polarity across the [[cell membrane|membrane]] of the axon. In response to a signal from another [[neuron]], sodium- (Na⁺) and potassium- (K⁺) gated [[Voltage-gated ion channel|ion channels]] open and close as the membrane reaches its [[threshold potential]]. Na⁺ channels open at the beginning of the action potential, and Na⁺ moves into the axon, causing [[depolarization]]. [[Repolarization]] occurs when the K⁺ channels open and K⁺ moves out of the axon, creating a change in polarity between the outside of the cell and the inside. The impulse travels down the axon in one direction only, to the [[axon terminal]] where it signals other neurons.|链接=Special:FilePath/Action_Potential.gif]]

[[File:Action Potential.gif|thumb|upright=1.5|As an action potential (nerve impulse) travels down an [[axon]] there is a change in polarity across the [[cell membrane|membrane]] of the axon. In response to a signal from another [[neuron]], sodium- (Na⁺) and potassium- (K⁺) gated [[Voltage-gated ion channel|ion channels]] open and close as the membrane reaches its [[threshold potential]]. Na⁺ channels open at the beginning of the action potential, and Na⁺ moves into the axon, causing [[depolarization]]. [[Repolarization]] occurs when the K⁺ channels open and K⁺ moves out of the axon, creating a change in polarity between the outside of the cell and the inside. The impulse travels down the axon in one direction only, to the [[axon terminal]] where it signals other neurons.|链接=Special:FilePath/Action_Potential.gif]]

In [[physiology]], an '''action potential''' ('''AP''') occurs when the [[membrane potential]] of a specific [[Cell (biology)|cell]] location rapidly rises and falls:<ref>{{cite journal | vauthors = Hodgkin AL, Huxley AF | title = A quantitative description of membrane current and its application to conduction and excitation in nerve | journal = The Journal of Physiology | volume = 117 | issue = 4 | pages = 500–44 | date = August 1952 | pmid = 12991237 | pmc = 1392413 | doi = 10.1113/jphysiol.1952.sp004764 }}</ref> this depolarization then causes adjacent locations to similarly depolarize. Action potentials occur in several types of [[animal cell]]s, called [[Membrane potential#Cell excitability|excitable]] cells, which include [[neuron]]s, [[myocyte|muscle cells]], [[endocrine]] cells and in some [[plant cell]]s.

In [[physiology]], an '''action potential''' ('''AP''') occurs when the [[membrane potential]] of a specific [[Cell (biology)|cell]] location rapidly rises and falls:<ref name=":3">{{cite journal | vauthors = Hodgkin AL, Huxley AF | title = A quantitative description of membrane current and its application to conduction and excitation in nerve | journal = The Journal of Physiology | volume = 117 | issue = 4 | pages = 500–44 | date = August 1952 | pmid = 12991237 | pmc = 1392413 | doi = 10.1113/jphysiol.1952.sp004764 }}</ref> this depolarization then causes adjacent locations to similarly depolarize. Action potentials occur in several types of [[animal cell]]s, called [[Membrane potential#Cell excitability|excitable]] cells, which include [[neuron]]s, [[myocyte|muscle cells]], [[endocrine]] cells and in some [[plant cell]]s.

In neurons, action potentials play a central role in [[cell–cell interaction|cell-to-cell communication]] by providing for—or with regard to [[saltatory conduction]], assisting—the propagation of signals along the neuron's [[axon]] toward [[axon terminal|synaptic boutons]] situated at the ends of an axon; these signals can then connect with other neurons at synapses, or to motor cells or glands. In other types of cells, their main function is to activate intracellular processes. In muscle cells, for example, an action potential is the first step in the chain of events leading to contraction. In [[beta cell]]s of the [[pancreas]], they provoke release of [[insulin]].<ref group="lower-alpha" name="pmid16464129">{{cite journal | vauthors = MacDonald PE, Rorsman P | title = Oscillations, intercellular coupling, and insulin secretion in pancreatic beta cells | journal = PLOS Biology | volume = 4 | issue = 2 | pages = e49 | date = February 2006 | pmid = 16464129 | pmc = 1363709 | doi = 10.1371/journal.pbio.0040049 }} {{open access}}</ref> Action potentials in neurons are also known as "'''nerve impulses'''" or "'''spikes'''", and the temporal sequence of action potentials generated by a neuron is called its "'''spike train'''". A neuron that emits an action potential, or nerve impulse, is often said to "fire".

In neurons, action potentials play a central role in [[cell–cell interaction|cell-to-cell communication]] by providing for—or with regard to [[saltatory conduction]], assisting—the propagation of signals along the neuron's [[axon]] toward [[axon terminal|synaptic boutons]] situated at the ends of an axon; these signals can then connect with other neurons at synapses, or to motor cells or glands. In other types of cells, their main function is to activate intracellular processes. In muscle cells, for example, an action potential is the first step in the chain of events leading to contraction. In [[beta cell]]s of the [[pancreas]], they provoke release of [[insulin]].<ref group="lower-alpha" name="pmid16464129">{{cite journal | vauthors = MacDonald PE, Rorsman P | title = Oscillations, intercellular coupling, and insulin secretion in pancreatic beta cells | journal = PLOS Biology | volume = 4 | issue = 2 | pages = e49 | date = February 2006 | pmid = 16464129 | pmc = 1363709 | doi = 10.1371/journal.pbio.0040049 }} {{open access}}</ref> Action potentials in neurons are also known as "'''nerve impulses'''" or "'''spikes'''", and the temporal sequence of action potentials generated by a neuron is called its "'''spike train'''". A neuron that emits an action potential, or nerve impulse, is often said to "fire".

神经元中，动作电位在细胞与细胞之间的通讯中起着中心作用，它提供ー或与跳跃式传导有关，协助信号沿着神经元的轴突向位于轴突末端的突触结传播；这些信号然后接触到突触的其他神经元、运动细胞或腺体。在其他类型的细胞中，它们的主要功能是激活细胞内的反应过程。例如，在肌肉细胞中，动作电位是导致肌肉收缩的一系列事件中的第一步。在胰腺的 β 细胞中，它们会刺激胰岛素的释放。神经元的动作电位也被称为“神经冲动”或“脉冲”，神经元产生的动作电位的时间序列被称为“动作电位序列”。神经元发出动作电位或神经冲动，也常说“发放”。

神经元中，动作电位在细胞与细胞之间的通讯中起着中心作用，它提供ー或与跳跃式传导有关，协助信号沿着神经元的轴突向位于轴突末端的突触结传播；这些信号然后接触到突触的其他神经元、运动细胞或腺体。在其他类型的细胞中，它们的主要功能是激活细胞内的反应过程。例如，在肌肉细胞中，动作电位是导致肌肉收缩的一系列事件中的第一步。在胰腺的 β 细胞中，它们会刺激胰岛素的释放<ref name="pmid16464129" group="lower-alpha" />。神经元的动作电位也被称为“神经冲动”或“脉冲”，神经元产生的动作电位的时间序列被称为“动作电位序列”。神经元发出动作电位或神经冲动，也常说“发放”。

Action potentials are generated by special types of [[voltage-gated ion channel]]s embedded in a cell's [[plasma membrane]].<ref name="pmid17515599" group=lower-alpha>{{cite journal | vauthors = Barnett MW, Larkman PM | title = The action potential | journal = Practical Neurology | volume = 7 | issue = 3 | pages = 192–7 | date = June 2007 | pmid = 17515599 | url = http://pn.bmj.com/content/7/3/192.short | url-status = live | archive-url = https://web.archive.org/web/20110708074452/http://pn.bmj.com/content/7/3/192.short | df = dmy-all | archive-date = 8 July 2011 }}</ref> These channels are shut when the membrane potential is near the (negative) [[resting potential]] of the cell, but they rapidly begin to open if the membrane potential increases to a precisely defined threshold voltage, [[depolarization|depolarising]] the transmembrane potential.<ref name="pmid17515599" group=lower-alpha /> When the channels open, they allow an inward flow of [[sodium]] ions, which changes the electrochemical gradient, which in turn produces a further rise in the membrane potential towards zero. This then causes more channels to open, producing a greater electric current across the cell membrane and so on. The process proceeds explosively until all of the available ion channels are open, resulting in a large upswing in the membrane potential. The rapid influx of sodium ions causes the polarity of the plasma membrane to reverse, and the ion channels then rapidly inactivate. As the sodium channels close, sodium ions can no longer enter the neuron, and they are then actively transported back out of the plasma membrane. [[Potassium]] channels are then activated, and there is an outward current of potassium ions, returning the electrochemical gradient to the resting state. After an action potential has occurred, there is a transient negative shift, called the [[afterhyperpolarization]].

Action potentials are generated by special types of [[voltage-gated ion channel]]s embedded in a cell's [[plasma membrane]].<ref name="pmid17515599" group=lower-alpha>{{cite journal | vauthors = Barnett MW, Larkman PM | title = The action potential | journal = Practical Neurology | volume = 7 | issue = 3 | pages = 192–7 | date = June 2007 | pmid = 17515599 | url = http://pn.bmj.com/content/7/3/192.short | url-status = live | archive-url = https://web.archive.org/web/20110708074452/http://pn.bmj.com/content/7/3/192.short | df = dmy-all | archive-date = 8 July 2011 }}</ref> These channels are shut when the membrane potential is near the (negative) [[resting potential]] of the cell, but they rapidly begin to open if the membrane potential increases to a precisely defined threshold voltage, [[depolarization|depolarising]] the transmembrane potential.<ref name="pmid17515599" group=lower-alpha /> When the channels open, they allow an inward flow of [[sodium]] ions, which changes the electrochemical gradient, which in turn produces a further rise in the membrane potential towards zero. This then causes more channels to open, producing a greater electric current across the cell membrane and so on. The process proceeds explosively until all of the available ion channels are open, resulting in a large upswing in the membrane potential. The rapid influx of sodium ions causes the polarity of the plasma membrane to reverse, and the ion channels then rapidly inactivate. As the sodium channels close, sodium ions can no longer enter the neuron, and they are then actively transported back out of the plasma membrane. [[Potassium]] channels are then activated, and there is an outward current of potassium ions, returning the electrochemical gradient to the resting state. After an action potential has occurred, there is a transient negative shift, called the [[afterhyperpolarization]].

In animal cells, there are two primary types of action potentials. One type is generated by [[voltage-gated sodium channels]], the other by voltage-gated [[calcium]] channels. Sodium-based action potentials usually last for under one millisecond, but calcium-based action potentials may last for 100 milliseconds or longer.{{citation needed|date=August 2020}} In some types of neurons, slow calcium spikes provide the driving force for a long burst of rapidly emitted sodium spikes. In [[cardiac action potential|cardiac muscle cells]], on the other hand, an initial fast sodium spike provides a "primer" to provoke the rapid onset of a calcium spike, which then produces muscle contraction.<ref>{{cite web |url=https://www.zoology.ubc.ca/~gardner/cardiac_muscle_contraction.htm#muscle_ap |title=Cardiac Muscle Contraction |accessdate=2021-05-28 }}</ref>

In animal cells, there are two primary types of action potentials. One type is generated by [[voltage-gated sodium channels]], the other by voltage-gated [[calcium]] channels. Sodium-based action potentials usually last for under one millisecond, but calcium-based action potentials may last for 100 milliseconds or longer.{{citation needed|date=August 2020}} In some types of neurons, slow calcium spikes provide the driving force for a long burst of rapidly emitted sodium spikes. In [[cardiac action potential|cardiac muscle cells]], on the other hand, an initial fast sodium spike provides a "primer" to provoke the rapid onset of a calcium spike, which then produces muscle contraction.<ref name=":4">{{cite web |url=https://www.zoology.ubc.ca/~gardner/cardiac_muscle_contraction.htm#muscle_ap |title=Cardiac Muscle Contraction |accessdate=2021-05-28 }}</ref>

==Overview 概述==

==Overview 概述==

[[File:Action potential basic shape.svg|thumb|right|Shape of a typical action potential. The membrane potential remains near a baseline level until at some point in time, it abruptly spikes upward and then rapidly falls.一个典型的动作电位的形状。膜电位一直保持在接近基线水平，直到某个时间点突然上升，然后迅速下降。|链接=Special:FilePath/Action_potential_basic_shape.svg]]

[[File:Action potential basic shape.svg|thumb|right|Shape of a typical action potential. The membrane potential remains near a baseline level until at some point in time, it abruptly spikes upward and then rapidly falls.一个典型的动作电位的形状。膜电位一直保持在接近基线水平，直到某个时间点突然上升，然后迅速下降。|链接=Special:FilePath/Action_potential_basic_shape.svg]]

Nearly all [[cell membrane]]s in animals, plants and fungi maintain a [[voltage]] difference between the exterior and interior of the cell, called the [[membrane potential]]. A typical voltage across an animal cell membrane is −70 mV. This means that the interior of the cell has a negative voltage relative to the exterior. In most types of cells, the membrane potential usually stays fairly constant. Some types of cells, however, are electrically active in the sense that their voltages fluctuate over time. In some types of electrically active cells, including [[neuron]]s and muscle cells, the voltage fluctuations frequently take the form of a rapid upward spike followed by a rapid fall. These up-and-down cycles are known as ''action potentials''. In some types of neurons, the entire up-and-down cycle takes place in a few thousandths of a second. In muscle cells, a typical action potential lasts about a fifth of a second. In some other types of cells and plants, an action potential may last three seconds or more.<ref>{{Cite journal|last=Pickard|first=Barbara | name-list-style = vanc |date=June 1973|title=Action Potentials in Higher Plants|url=http://www.esalq.usp.br/lepse/imgs/conteudo_thumb/Action-Potentials-in-Higher-Plants-1.pdf|journal=The Botanical Review|volume=39|issue=2|pages=188|doi=10.1007/BF02859299|s2cid=5026557 }}</ref>

Nearly all [[cell membrane]]s in animals, plants and fungi maintain a [[voltage]] difference between the exterior and interior of the cell, called the [[membrane potential]]. A typical voltage across an animal cell membrane is −70 mV. This means that the interior of the cell has a negative voltage relative to the exterior. In most types of cells, the membrane potential usually stays fairly constant. Some types of cells, however, are electrically active in the sense that their voltages fluctuate over time. In some types of electrically active cells, including [[neuron]]s and muscle cells, the voltage fluctuations frequently take the form of a rapid upward spike followed by a rapid fall. These up-and-down cycles are known as ''action potentials''. In some types of neurons, the entire up-and-down cycle takes place in a few thousandths of a second. In muscle cells, a typical action potential lasts about a fifth of a second. In some other types of cells and plants, an action potential may last three seconds or more.<ref name=":5">{{Cite journal|last=Pickard|first=Barbara | name-list-style = vanc |date=June 1973|title=Action Potentials in Higher Plants|url=http://www.esalq.usp.br/lepse/imgs/conteudo_thumb/Action-Potentials-in-Higher-Plants-1.pdf|journal=The Botanical Review|volume=39|issue=2|pages=188|doi=10.1007/BF02859299|s2cid=5026557 }}</ref>

几乎所有动物、植物和真菌的细胞膜在细胞外部和内部保持电压差，称为膜电位。通过动物细胞膜的典型电压是 -70mv。这意味着电池的内部相对于外部有一个负电压。在大多数类型的细胞中，膜电位通常保持相当稳定。然而，某些类型的电池是电活跃的，因为它们的电压随着时间而波动。在某些类型的电活性细胞中，包括神经元和肌肉细胞，电压波动通常表现为一个迅速上升的尖峰，然后迅速下降。这些上下周期被称为动作电位。在某些类型的神经元中，整个上下周期发生在千分之几秒内。在肌肉细胞中，典型的动作电位持续时间约为五分之一秒。在其他类型的细胞和植物中，动作电位可能持续三秒或更长时间。

几乎所有动物、植物和真菌的细胞膜在细胞外部和内部保持电压差，称为膜电位。通过动物细胞膜的典型电压是 -70mv。这意味着电池的内部相对于外部有一个负电压。在大多数类型的细胞中，膜电位通常保持相当稳定。然而，某些类型的电池是电活跃的，因为它们的电压随着时间而波动。在某些类型的电活性细胞中，包括神经元和肌肉细胞，电压波动通常表现为一个迅速上升的尖峰，然后迅速下降。这些上下周期被称为动作电位。在某些类型的神经元中，整个上下周期发生在千分之几秒内。在肌肉细胞中，典型的动作电位持续时间约为五分之一秒。在其他类型的细胞和植物中，动作电位可能持续三秒或更长时间。.<ref name=":5" />

The electrical properties of a cell are determined by the structure of the membrane that surrounds it. A [[cell membrane]] consists of a [[lipid bilayer]] of molecules in which larger protein molecules are embedded. The lipid bilayer is highly resistant to movement of electrically charged ions, so it functions as an insulator. The large membrane-embedded proteins, in contrast, provide channels through which ions can pass across the membrane. Action potentials are driven by channel proteins whose configuration switches between closed and open states as a function of the voltage difference between the interior and exterior of the cell. These voltage-sensitive proteins are known as [[voltage-gated ion channel]]s.

The electrical properties of a cell are determined by the structure of the membrane that surrounds it. A [[cell membrane]] consists of a [[lipid bilayer]] of molecules in which larger protein molecules are embedded. The lipid bilayer is highly resistant to movement of electrically charged ions, so it functions as an insulator. The large membrane-embedded proteins, in contrast, provide channels through which ions can pass across the membrane. Action potentials are driven by channel proteins whose configuration switches between closed and open states as a function of the voltage difference between the interior and exterior of the cell. These voltage-sensitive proteins are known as [[voltage-gated ion channel]]s.

===Process in a typical neuron典型神经元过程===

===Process in a typical neuron典型神经元过程===

[[File:Action potential.svg|thumb|300px|Approximate plot of a typical action potential shows its various phases as the action potential passes a point on a [[cell membrane]]. The membrane potential starts out at approximately −70 mV at time zero. A stimulus is applied at time = 1 ms, which raises the membrane potential above −55 mV (the threshold potential). After the stimulus is applied, the membrane potential rapidly rises to a peak potential of +40 mV at time = 2 ms. Just as quickly, the potential then drops and overshoots to −90 mV at time = 3 ms, and finally the resting potential of −70 mV is reestablished at time = 5 ms.|链接=Special:FilePath/Action_potential.svg]]

[[File:Action potential.svg|thumb|300px|Approximate plot of a typical action potential shows its various phases as the action potential passes a point on a [[cell membrane]]. The membrane potential starts out at approximately −70 mV at time zero. A stimulus is applied at time = 1 ms, which raises the membrane potential above −55 mV (the threshold potential). After the stimulus is applied, the membrane potential rapidly rises to a peak potential of +40 mV at time = 2 ms. Just as quickly, the potential then drops and overshoots to −90 mV at time = 3 ms, and finally the resting potential of −70 mV is reestablished at time = 5 ms.|链接=Special:FilePath/Action_potential.svg]]

All cells in animal body tissues are [[Dielectric#Ionic polarization|electrically polarized]] – in other words, they maintain a voltage difference across the cell's [[plasma membrane]], known as the [[membrane potential]]. This electrical polarization results from a complex interplay between protein structures embedded in the membrane called [[Ion transporter|ion pump]]s and [[ion channel]]s. In neurons, the types of ion channels in the membrane usually vary across different parts of the cell, giving the [[dendrite]]s, [[axon]], and [[soma (biology)|cell body]] different electrical properties. As a result, some parts of the membrane of a neuron may be excitable (capable of generating action potentials), whereas others are not. Recent studies have shown that the most excitable part of a neuron is the part after the [[axon hillock]] (the point where the axon leaves the cell body), which is called the [[axonal initial segment]], but the axon and cell body are also excitable in most cases.<ref>{{cite journal | vauthors = Leterrier C | title = The Axon Initial Segment: An Updated Viewpoint | journal = The Journal of Neuroscience | volume = 38 | issue = 9 | pages = 2135–2145 | date = February 2018 | pmid = 29378864 | pmc = 6596274 | doi = 10.1523/JNEUROSCI.1922-17.2018 }}</ref>

All cells in animal body tissues are [[Dielectric#Ionic polarization|electrically polarized]] – in other words, they maintain a voltage difference across the cell's [[plasma membrane]], known as the [[membrane potential]]. This electrical polarization results from a complex interplay between protein structures embedded in the membrane called [[Ion transporter|ion pump]]s and [[ion channel]]s. In neurons, the types of ion channels in the membrane usually vary across different parts of the cell, giving the [[dendrite]]s, [[axon]], and [[soma (biology)|cell body]] different electrical properties. As a result, some parts of the membrane of a neuron may be excitable (capable of generating action potentials), whereas others are not. Recent studies have shown that the most excitable part of a neuron is the part after the [[axon hillock]] (the point where the axon leaves the cell body), which is called the [[axonal initial segment]], but the axon and cell body are also excitable in most cases.<ref name=":6">{{cite journal | vauthors = Leterrier C | title = The Axon Initial Segment: An Updated Viewpoint | journal = The Journal of Neuroscience | volume = 38 | issue = 9 | pages = 2135–2145 | date = February 2018 | pmid = 29378864 | pmc = 6596274 | doi = 10.1523/JNEUROSCI.1922-17.2018 }}</ref>

动物身体组织中的所有细胞都是电极化的——换句话说，它们维持一个跨细胞质膜的电压差，即所谓的膜电位。这种电极化是嵌入在质膜的蛋白质结构(称为离子泵和离子通道)之间复杂的相互作用的结果。神经元中，细胞膜上的离子通道类型在细胞的不同部位有所不同，这使得树突、轴突和胞体具有不同的电特性。因此，神经元膜的某些部位是可兴奋的(能够产生动作电位) ，而其他部位则不是。近年来的研究表明，神经元最易兴奋的部位是轴丘(轴突离开细胞体的部位)之后的部位，称为轴突初始段，但在大多数情况下轴突和胞体也是可兴奋的。

动物身体组织中的所有细胞都是电极化的——换句话说，它们维持一个跨细胞质膜的电压差，即所谓的膜电位。这种电极化是嵌入在质膜的蛋白质结构(称为离子泵和离子通道)之间复杂的相互作用的结果。神经元中，细胞膜上的离子通道类型在细胞的不同部位有所不同，这使得树突、轴突和胞体具有不同的电特性。因此，神经元膜的某些部位是可兴奋的(能够产生动作电位) ，而其他部位则不是。近年来的研究表明，神经元最易兴奋的部位是轴丘(轴突离开细胞体的部位)之后的部位，称为轴突初始段，但在大多数情况下轴突和胞体也是可兴奋的。s.<ref name=":6" />

Each excitable patch of membrane has two important levels of membrane potential: the [[resting potential]], which is the value the membrane potential maintains as long as nothing perturbs the cell, and a higher value called the [[threshold potential]]. At the axon hillock of a typical neuron, the resting potential is around –70 millivolts (mV) and the threshold potential is around –55 mV. Synaptic inputs to a neuron cause the membrane to [[depolarization|depolarize]] or [[Hyperpolarization (biology)|hyperpolarize]]; that is, they cause the membrane potential to rise or fall. Action potentials are triggered when enough depolarization accumulates to bring the membrane potential up to threshold. When an action potential is triggered, the membrane potential abruptly shoots upward and then equally abruptly shoots back downward, often ending below the resting level, where it remains for some period of time. The shape of the action potential is stereotyped; this means that the rise and fall usually have approximately the same amplitude and time course for all action potentials in a given cell. (Exceptions are discussed later in the article). In most neurons, the entire process takes place in about a thousandth of a second. Many types of neurons emit action potentials constantly at rates of up to 10–100 per second. However, some types are much quieter, and may go for minutes or longer without emitting any action potentials.

Each excitable patch of membrane has two important levels of membrane potential: the [[resting potential]], which is the value the membrane potential maintains as long as nothing perturbs the cell, and a higher value called the [[threshold potential]]. At the axon hillock of a typical neuron, the resting potential is around –70 millivolts (mV) and the threshold potential is around –55 mV. Synaptic inputs to a neuron cause the membrane to [[depolarization|depolarize]] or [[Hyperpolarization (biology)|hyperpolarize]]; that is, they cause the membrane potential to rise or fall. Action potentials are triggered when enough depolarization accumulates to bring the membrane potential up to threshold. When an action potential is triggered, the membrane potential abruptly shoots upward and then equally abruptly shoots back downward, often ending below the resting level, where it remains for some period of time. The shape of the action potential is stereotyped; this means that the rise and fall usually have approximately the same amplitude and time course for all action potentials in a given cell. (Exceptions are discussed later in the article). In most neurons, the entire process takes place in about a thousandth of a second. Many types of neurons emit action potentials constantly at rates of up to 10–100 per second. However, some types are much quieter, and may go for minutes or longer without emitting any action potentials.

{{more citations needed section|date=February 2014}}

{{more citations needed section|date=February 2014}}

Action potentials result from the presence in a cell's membrane of special types of [[voltage-gated ion channel]]s.<ref>{{cite book |veditors=Purves D, Augustine GJ, Fitzpatrick D, et al |title=Neuroscience |edition=2nd |place=Sunderland, MA |publisher=Sinauer Associates |date=2001 |chapter=Voltage-Gated Ion Channels |chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK10883/ |access-date=2017-08-29 |url-status=live |archive-url=https://web.archive.org/web/20180605025823/https://www.ncbi.nlm.nih.gov/books/NBK10883/ |archive-date=5 June 2018 |df=dmy-all }}</ref> A voltage-gated ion channel is a transmembrane protein that has three key properties:

Action potentials result from the presence in a cell's membrane of special types of [[voltage-gated ion channel]]s.<ref name=":7">{{cite book |veditors=Purves D, Augustine GJ, Fitzpatrick D, et al |title=Neuroscience |edition=2nd |place=Sunderland, MA |publisher=Sinauer Associates |date=2001 |chapter=Voltage-Gated Ion Channels |chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK10883/ |access-date=2017-08-29 |url-status=live |archive-url=https://web.archive.org/web/20180605025823/https://www.ncbi.nlm.nih.gov/books/NBK10883/ |archive-date=5 June 2018 |df=dmy-all }}</ref> A voltage-gated ion channel is a transmembrane protein that has three key properties:

#It is capable of assuming more than one conformation.

#It is capable of assuming more than one conformation.

#At least one of the conformations creates a channel through the membrane that is permeable to specific types of ions.

#At least one of the conformations creates a channel through the membrane that is permeable to specific types of ions.

#The transition between conformations is influenced by the membrane potential.

#The transition between conformations is influenced by the membrane potential.

#它能够呈现多个构象。

#它能够呈现多个构象。

#至少其中一种构象在膜上形成一个通道，可以渗透特定种类的离子。

#至少其中一种构象在膜上形成一个通道，可以渗透特定种类的离子。

The most intensively studied type of voltage-dependent ion channels comprises the sodium channels involved in fast nerve conduction. These are sometimes known as Hodgkin-Huxley sodium channels because they were first characterized by [[Alan Lloyd Hodgkin|Alan Hodgkin]] and [[Andrew Huxley]] in their Nobel Prize-winning studies of the biophysics of the action potential, but can more conveniently be referred to as ''Na''_V channels. (The "V" stands for "voltage".) An ''Na''_V channel has three possible states, known as ''deactivated'', ''activated'', and ''inactivated''. The channel is permeable only to sodium ions when it is in the ''activated'' state. When the membrane potential is low, the channel spends most of its time in the ''deactivated'' (closed) state. If the membrane potential is raised above a certain level, the channel shows increased probability of transitioning to the ''activated'' (open) state. The higher the membrane potential the greater the probability of activation. Once a channel has activated, it will eventually transition to the ''inactivated'' (closed) state. It tends then to stay inactivated for some time, but, if the membrane potential becomes low again, the channel will eventually transition back to the ''deactivated'' state. During an action potential, most channels of this type go through a cycle ''deactivated''→''activated''→''inactivated''→''deactivated''. This is only the population average behavior, however – an individual channel can in principle make any transition at any time. However, the likelihood of a channel's transitioning from the ''inactivated'' state directly to the ''activated'' state is very low: A channel in the ''inactivated'' state is refractory until it has transitioned back to the ''deactivated'' state.

The most intensively studied type of voltage-dependent ion channels comprises the sodium channels involved in fast nerve conduction. These are sometimes known as Hodgkin-Huxley sodium channels because they were first characterized by [[Alan Lloyd Hodgkin|Alan Hodgkin]] and [[Andrew Huxley]] in their Nobel Prize-winning studies of the biophysics of the action potential, but can more conveniently be referred to as ''Na''_V channels. (The "V" stands for "voltage".) An ''Na''_V channel has three possible states, known as ''deactivated'', ''activated'', and ''inactivated''. The channel is permeable only to sodium ions when it is in the ''activated'' state. When the membrane potential is low, the channel spends most of its time in the ''deactivated'' (closed) state. If the membrane potential is raised above a certain level, the channel shows increased probability of transitioning to the ''activated'' (open) state. The higher the membrane potential the greater the probability of activation. Once a channel has activated, it will eventually transition to the ''inactivated'' (closed) state. It tends then to stay inactivated for some time, but, if the membrane potential becomes low again, the channel will eventually transition back to the ''deactivated'' state. During an action potential, most channels of this type go through a cycle ''deactivated''→''activated''→''inactivated''→''deactivated''. This is only the population average behavior, however – an individual channel can in principle make any transition at any time. However, the likelihood of a channel's transitioning from the ''inactivated'' state directly to the ''activated'' state is very low: A channel in the ''inactivated'' state is refractory until it has transitioned back to the ''deactivated'' state.

研究最多的电压依赖型离子通道包括参与快速神经传导的钠通道。这些钠离子通道有时被称为 Hodgkin-Huxley 钠离子通道，因为它们是 Alan Hodgkin 和 Andrew Huxley 在他们获得诺贝尔奖的动作电位的生物物理学研究中第一个描述的，但是更方便地被称为 ''Na''_V  通道。(“ v”代表“电压”。)''Na''_V  通道有三种可能的状态，被称为失活、激活和灭活。当通道处于激活状态时，它只能透过钠离子。当膜电位低时，通道大部分时间处于非激活(关闭)状态。如果膜电位升高到某一水平以上，通道转换到激活(开放)状态的概率增加。膜电位越高，激活的可能性就越大。一旦通道被激活，它最终将转换到灭活(关闭)状态。然后它趋向于在一段时间内保持灭活状态，但是，如果膜电位再次变低，通道最终会转换到失活状态。在动作电位发生过程中，大多数这种类型的通道经历一个循环 失活→激活→灭活→失活的过程。然而这只是群体平均行为——在理论上单个通道可以在任何时间进行任何转换。然而，通道从灭活状态直接转换到激活状态的可能性非常低：处于灭活状态的通道是不应的，直到它回到灭活状态。

研究最多的电压依赖型离子通道包括参与快速神经传导的钠通道。这些钠离子通道有时被称为 Hodgkin-Huxley 钠离子通道，因为它们是 Alan Hodgkin 和 Andrew Huxley 在他们获得诺贝尔奖的动作电位的生物物理学研究中第一个描述的，但是更方便地被称为 ''Na''_V  通道(“ v”代表“电压”)。''Na''_V  通道有三种可能的状态，被称为失活、激活和灭活。当通道处于激活状态时，它只能透过钠离子。当膜电位低时，通道大部分时间处于非激活(关闭)状态。如果膜电位升高到某一水平以上，通道转换到激活(开放)状态的概率增加。膜电位越高，激活的可能性就越大。一旦通道被激活，它最终将转换到灭活(关闭)状态。然后它趋向于在一段时间内保持灭活状态，但是，如果膜电位再次变低，通道最终会转换到失活状态。在动作电位发生过程中，大多数这种类型的通道经历一个循环 失活→激活→灭活→失活的过程。然而这只是群体平均行为——在理论上单个通道可以在任何时间进行任何转换。然而，通道从灭活状态直接转换到激活状态的可能性非常低：处于灭活状态的通道是不应的，直到它回到灭活状态。

The outcome of all this is that the kinetics of the ''Na''_V channels are governed by a transition matrix whose rates are voltage-dependent in a complicated way. Since these channels themselves play a major role in determining the voltage, the global dynamics of the system can be quite difficult to work out. Hodgkin and Huxley approached the problem by developing a set of [[differential equation]]s for the parameters that govern the ion channel states, known as the [[Hodgkin–Huxley model|Hodgkin-Huxley equations]]. These equations have been extensively modified by later research, but form the starting point for most theoretical studies of action potential biophysics.

The outcome of all this is that the kinetics of the ''Na''_V channels are governed by a transition matrix whose rates are voltage-dependent in a complicated way. Since these channels themselves play a major role in determining the voltage, the global dynamics of the system can be quite difficult to work out. Hodgkin and Huxley approached the problem by developing a set of [[differential equation]]s for the parameters that govern the ion channel states, known as the [[Hodgkin–Huxley model|Hodgkin-Huxley equations]]. These equations have been extensively modified by later research, but form the starting point for most theoretical studies of action potential biophysics.

所有这一切的结果是，''Na''_V 通道的动力学由一个转移矩阵控制，它的速率以一种复杂的方式依赖于电压。由于这些通道本身在决定电压方面起着重要作用，系统的全局动力学可能很难计算出来。为了解决这个问题，Hodgkin 和 Huxley 为控制离子通道状态的参数建立了一组微分方程，称为 Hodgkin-Huxley 方程。这些方程在后来的研究中得到了广泛的修正，但却成为了动作势生物物理学大多数理论研究的出发点。

所有这一切的结果是，''Na''_V 通道的动力学受制于一个转移矩阵，它的速率以一种复杂的方式依赖于电压。由于这些通道本身在决定电位方面起着重要作用，系统的全局动力学可能很难计算出来。为了解决这个问题，Hodgkin 和 Huxley 为控制离子通道状态的参数建立了一组微分方程，称为 Hodgkin-Huxley 方程。这些方程在后来的研究中得到了广泛的修正，但却成为了动作电位生物物理学大多数理论研究的出发点。

[[File:Membrane Permeability of a Neuron During an Action Potential.svg|thumb|upright=1.75|right|Ion movement during an action potential.<br />''Key:'' a) Sodium (Na⁺) ion. b) Potassium (K⁺) ion. c) Sodium channel. d) Potassium channel. e) Sodium-potassium pump.<br/> In the stages of an action potential, the permeability of the membrane of the neuron changes. At the '''resting state''' (1), sodium and potassium ions have limited ability to pass through the membrane, and the neuron has a net negative charge inside. Once the action potential is triggered, the '''depolarization''' (2) of the neuron activates sodium channels, allowing sodium ions to pass through the cell membrane into the cell, resulting in a net positive charge in the neuron relative to the extracellular fluid. After the action potential peak is reached, the neuron begins '''repolarization''' (3), where the sodium channels close and potassium channels open, allowing potassium ions to cross the membrane into the extracellular fluid, returning the membrane potential to a negative value. Finally, there is a '''refractory period''' (4), during which the voltage-dependent ion channels are [[Voltage-gated ion channel#Mechanism|inactivated]] while the Na⁺ and K⁺ ions return to their resting state distributions across the membrane (1), and the neuron is ready to repeat the process for the next action potential.|链接=Special:FilePath/Membrane_Permeability_of_a_Neuron_During_an_Action_Potential.svg]]

[[File:Membrane Permeability of a Neuron During an Action Potential.svg|thumb|upright=1.75|right|Ion movement during an action potential.<br />''Key:'' a) Sodium (Na⁺) ion. b) Potassium (K⁺) ion. c) Sodium channel. d) Potassium channel. e) Sodium-potassium pump.<br/> In the stages of an action potential, the permeability of the membrane of the neuron changes. At the '''resting state''' (1), sodium and potassium ions have limited ability to pass through the membrane, and the neuron has a net negative charge inside. Once the action potential is triggered, the '''depolarization''' (2) of the neuron activates sodium channels, allowing sodium ions to pass through the cell membrane into the cell, resulting in a net positive charge in the neuron relative to the extracellular fluid. After the action potential peak is reached, the neuron begins '''repolarization''' (3), where the sodium channels close and potassium channels open, allowing potassium ions to cross the membrane into the extracellular fluid, returning the membrane potential to a negative value. Finally, there is a '''refractory period''' (4), during which the voltage-dependent ion channels are [[Voltage-gated ion channel#Mechanism|inactivated]] while the Na⁺ and K⁺ ions return to their resting state distributions across the membrane (1), and the neuron is ready to repeat the process for the next action potential.|链接=Special:FilePath/Membrane_Permeability_of_a_Neuron_During_an_Action_Potential.svg]]

As the membrane potential is increased, [[sodium channel|sodium ion channels]] open, allowing the entry of [[sodium]] ions into the cell. This is followed by the opening of [[potassium channel|potassium ion channels]] that permit the exit of [[potassium]] ions from the cell. The inward flow of sodium ions increases the concentration of positively charged [[cation]]s in the cell and causes depolarization, where the potential of the cell is higher than the cell's [[resting potential]]. The sodium channels close at the peak of the action potential, while potassium continues to leave the cell. The efflux of potassium ions decreases the membrane potential or hyperpolarizes the cell. For small voltage increases from rest, the potassium current exceeds the sodium current and the voltage returns to its normal resting value, typically −70&nbsp;mV.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfn|Junge|1981|pp=89–90}}{{sfn|Schmidt-Nielsen|1997|p=484}} However, if the voltage increases past a critical threshold, typically 15&nbsp;mV higher than the resting value, the sodium current dominates. This results in a runaway condition whereby the [[positive feedback]] from the sodium current activates even more sodium channels. Thus, the cell ''fires'', producing an action potential.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=48–49|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2p=141|3a1=Schmidt-Nielsen|3y=1997|3p=483|4a1=Junge|4y=1981|4p=89}}{{sfn|Stevens|1966|p=127}}{{refn|In general, while this simple description of action potential initiation is accurate, it does not explain phenomena such as excitation block (the ability to prevent neurons from eliciting action potentials by stimulating them with large current steps) and the ability to elicit action potentials by briefly hyperpolarizing the membrane. By analyzing the dynamics of a system of sodium and potassium channels in a membrane patch using [[computational model]]s, however, these phenomena are readily explained.<ref group=lower-Greek>{{cite journal|title=FitzHugh-Nagumo model|journal=Scholarpedia|volume=1|issue=9|pages=1349|df=dmy-all|doi=10.4249/scholarpedia.1349|year=2006|last1=Fitzhugh|first1=Richard|last2=Izhikevich|first2=Eugene | name-list-style = vanc |bibcode=2006SchpJ...1.1349I|doi-access=free}}</ref>|group="note"}} The frequency at which a neuron elicits action potentials is often referred to as a '''firing rate''' or '''neural firing rate'''.<!--"Neural firing rate" redirects here; these terms are bolded per MOS:BOLD.-->

As the membrane potential is increased, [[sodium channel|sodium ion channels]] open, allowing the entry of [[sodium]] ions into the cell. This is followed by the opening of [[potassium channel|potassium ion channels]] that permit the exit of [[potassium]] ions from the cell. The inward flow of sodium ions increases the concentration of positively charged [[cation]]s in the cell and causes depolarization, where the potential of the cell is higher than the cell's [[resting potential]]. The sodium channels close at the peak of the action potential, while potassium continues to leave the cell. The efflux of potassium ions decreases the membrane potential or hyperpolarizes the cell. For small voltage increases from rest, the potassium current exceeds the sodium current and the voltage returns to its normal resting value, typically −70&nbsp;mV.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfn|Junge|1981|pp=89–90}}{{sfn|Schmidt-Nielsen|1997|p=484}} However, if the voltage increases past a critical threshold, typically 15&nbsp;mV higher than the resting value, the sodium current dominates. This results in a runaway condition whereby the [[positive feedback]] from the sodium current activates even more sodium channels. Thus, the cell ''fires'', producing an action potential.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=48–49|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2p=141|3a1=Schmidt-Nielsen|3y=1997|3p=483|4a1=Junge|4y=1981|4p=89}}{{sfn|Stevens|1966|p=127}}{{refn|In general, while this simple description of action potential initiation is accurate, it does not explain phenomena such as excitation block (the ability to prevent neurons from eliciting action potentials by stimulating them with large current steps) and the ability to elicit action potentials by briefly hyperpolarizing the membrane. By analyzing the dynamics of a system of sodium and potassium channels in a membrane patch using [[computational model]]s, however, these phenomena are readily explained.<ref group=lower-Greek>{{cite journal|title=FitzHugh-Nagumo model|journal=Scholarpedia|volume=1|issue=9|pages=1349|df=dmy-all|doi=10.4249/scholarpedia.1349|year=2006|last1=Fitzhugh|first1=Richard|last2=Izhikevich|first2=Eugene | name-list-style = vanc |bibcode=2006SchpJ...1.1349I|doi-access=free}}</ref>|group="note"}} The frequency at which a neuron elicits action potentials is often referred to as a '''firing rate''' or '''neural firing rate'''.<!--"Neural firing rate" redirects here; these terms are bolded per MOS:BOLD.-->

随着膜电位的增加，钠离子通道打开，允许钠离子进入细胞。其次是开放钾离子通道，允许钾离子从细胞出口。钠离子的内向流动增加了细胞中正电荷阳离子的浓度，导致去极化，这时细胞的电位高于细胞的静息电位。钠离子通道在动作电位峰值处关闭，而钾离子继续离开细胞。钾离子的外流会降低细胞的膜电位或使细胞超极化。对于静止的小电压增加，钾电流超过钠电流，电压恢复到正常的静止值，通常为 -70 mV。然而，如果电压增加超过一个临界阈值，通常高于静息值15毫伏，钠电流占主导地位。这就导致了一种失控的情况，即钠电流的正反馈激活了更多的钠通道。因此，细胞被激活，产生动作电位。神经元诱发动作电位的频率通常被称为放电频率或神经放电频率。

随着膜电位的增加，钠离子通道打开，允许钠离子进入细胞。其次是开放钾离子通道，允许钾离子流出细胞。钠离子内流增加了细胞中正电荷阳离子的浓度，导致去极化，这时细胞的电位高于细胞的静息电位。钠离子通道在动作电位峰值处关闭，而钾离子继续流出细胞。钾离子外流会降低细胞的膜电位或使细胞超极化。从静息电位小幅增加的电位，钾电流超过钠电流，电压恢复到正常的静息值，通常为 -70 mV。然而，如果电位增加超过一个临界阈值，通常高于静息值15毫伏，钠电流将占主导地位。这就导致了一种失控的情况，即钠电流的正反馈激活了更多的钠通道。因此，细胞发放，产生动作电位。神经元诱发动作电位的频率通常被称为发放频率或神经放电频率。

Currents produced by the opening of voltage-gated channels in the course of an action potential are typically significantly larger than the initial stimulating current. Thus, the amplitude, duration, and shape of the action potential are determined largely by the properties of the excitable membrane and not the amplitude or duration of the stimulus. This [[All-or-none law|all-or-nothing]] property of the action potential sets it apart from [[graded potential]]s such as [[receptor potential]]s, [[electrotonic potential]]s, [[subthreshold membrane potential oscillations]], and [[synaptic potential]]s, which scale with the magnitude of the stimulus. A variety of action potential types exist in many cell types and cell compartments as determined by the types of voltage-gated channels, [[leak channels]], channel distributions, ionic concentrations, membrane capacitance, temperature, and other factors.

Currents produced by the opening of voltage-gated channels in the course of an action potential are typically significantly larger than the initial stimulating current. Thus, the amplitude, duration, and shape of the action potential are determined largely by the properties of the excitable membrane and not the amplitude or duration of the stimulus. This [[All-or-none law|all-or-nothing]] property of the action potential sets it apart from [[graded potential]]s such as [[receptor potential]]s, [[electrotonic potential]]s, [[subthreshold membrane potential oscillations]], and [[synaptic potential]]s, which scale with the magnitude of the stimulus. A variety of action potential types exist in many cell types and cell compartments as determined by the types of voltage-gated channels, [[leak channels]], channel distributions, ionic concentrations, membrane capacitance, temperature, and other factors.

The principal ions involved in an action potential are sodium and potassium cations; sodium ions enter the cell, and potassium ions leave, restoring equilibrium. Relatively few ions need to cross the membrane for the membrane voltage to change drastically. The ions exchanged during an action potential, therefore, make a negligible change in the interior and exterior ionic concentrations. The few ions that do cross are pumped out again by the continuous action of the [[sodium–potassium pump]], which, with other [[ion transporter]]s, maintains the normal ratio of ion concentrations across the membrane. [[Calcium]] cations and [[chloride]] [[anion]]s are involved in a few types of action potentials, such as the [[cardiac action potential]] and the action potential in the single-cell [[algae|alga]] ''[[Acetabularia]]'', respectively.

The principal ions involved in an action potential are sodium and potassium cations; sodium ions enter the cell, and potassium ions leave, restoring equilibrium. Relatively few ions need to cross the membrane for the membrane voltage to change drastically. The ions exchanged during an action potential, therefore, make a negligible change in the interior and exterior ionic concentrations. The few ions that do cross are pumped out again by the continuous action of the [[sodium–potassium pump]], which, with other [[ion transporter]]s, maintains the normal ratio of ion concentrations across the membrane. [[Calcium]] cations and [[chloride]] [[anion]]s are involved in a few types of action potentials, such as the [[cardiac action potential]] and the action potential in the single-cell [[algae|alga]] ''[[Acetabularia]]'', respectively.

与动作电位有关的主要离子是钠离子和钾离子; 钠离子进入细胞，钾离子离开，恢复平衡。相对而言，只有很少的离子需要穿过膜电位膜才能发生剧烈的变化。因此，在动作电位期间交换的离子在内部和外部离子浓度中的变化微不足道。少数交叉的离子通过钠钾泵的连续作用再次泵出，钠钾泵与其他离子输送器一起，维持了跨膜离子浓度的正常比例。钙离子和氯离子参与了几种类型的动作电位，如心脏动作电位和髋臼单细胞动作电位。

与动作电位有关的主要离子是钠离子和钾离子; 钠离子进入细胞，钾离子离开，恢复平衡。只需相对很少的离子跨膜就能引起膜电位剧烈的变化。因此，在动作电位期间交换的离子对内部和外部离子浓度的改变微不足道。少数跨膜的离子通过钠钾泵的连续作用再次泵出，钠钾泵与其他离子转运蛋白一起，维持了跨膜离子浓度的正常比例。钙离子和氯离子参与了几种类型的动作电位，比如分别参与心肌动作电位和单细胞的伞藻的动作电位。

Although action potentials are generated locally on patches of excitable membrane, the resulting currents can trigger action potentials on neighboring stretches of membrane, precipitating a domino-like propagation. In contrast to passive spread of electric potentials ([[electrotonic potential]]), action potentials are generated anew along excitable stretches of membrane and propagate without decay.<ref name="no_decrement">[[Knut Schmidt-Nielsen|Schmidt-Nielsen]], p. 484.</ref> Myelinated sections of axons are not excitable and do not produce action potentials and the signal is propagated passively as [[electrotonic potential]]. Regularly spaced unmyelinated patches, called the [[nodes of Ranvier]], generate action potentials to boost the signal. Known as [[saltatory conduction]], this type of signal propagation provides a favorable tradeoff of signal velocity and axon diameter. Depolarization of [[axon terminal]]s, in general, triggers the release of [[neurotransmitter]] into the [[synaptic cleft]]. In addition, backpropagating action potentials have been recorded in the dendrites of [[pyramidal cell|pyramidal neurons]], which are ubiquitous in the neocortex.<ref name="backpropagation_in_pyramidal_cells" group=lower-alpha>{{cite journal | vauthors = Golding NL, Kath WL, Spruston N | title = Dichotomy of action-potential backpropagation in CA1 pyramidal neuron dendrites | journal = Journal of Neurophysiology | volume = 86 | issue = 6 | pages = 2998–3010 | date = December 2001 | pmid = 11731556 | doi = 10.1152/jn.2001.86.6.2998 | s2cid = 2915815 | df = dmy-all }}</ref> These are thought to have a role in [[spike-timing-dependent plasticity]].

Although action potentials are generated locally on patches of excitable membrane, the resulting currents can trigger action potentials on neighboring stretches of membrane, precipitating a domino-like propagation. In contrast to passive spread of electric potentials ([[electrotonic potential]]), action potentials are generated anew along excitable stretches of membrane and propagate without decay.<ref name="no_decrement">[[Knut Schmidt-Nielsen|Schmidt-Nielsen]], p. 484.</ref> Myelinated sections of axons are not excitable and do not produce action potentials and the signal is propagated passively as [[electrotonic potential]]. Regularly spaced unmyelinated patches, called the [[nodes of Ranvier]], generate action potentials to boost the signal. Known as [[saltatory conduction]], this type of signal propagation provides a favorable tradeoff of signal velocity and axon diameter. Depolarization of [[axon terminal]]s, in general, triggers the release of [[neurotransmitter]] into the [[synaptic cleft]]. In addition, backpropagating action potentials have been recorded in the dendrites of [[pyramidal cell|pyramidal neurons]], which are ubiquitous in the neocortex.<ref name="backpropagation_in_pyramidal_cells" group=lower-alpha>{{cite journal | vauthors = Golding NL, Kath WL, Spruston N | title = Dichotomy of action-potential backpropagation in CA1 pyramidal neuron dendrites | journal = Journal of Neurophysiology | volume = 86 | issue = 6 | pages = 2998–3010 | date = December 2001 | pmid = 11731556 | doi = 10.1152/jn.2001.86.6.2998 | s2cid = 2915815 | df = dmy-all }}</ref> These are thought to have a role in [[spike-timing-dependent plasticity]].

虽然动作电位是在可激活膜片上局部产生的，但由此产生的电流可以触发相邻膜片上的动作电位，促成多米诺骨牌般的传播。与被动传播的电位(电渗电位)不同，动作电位沿着可激活的细胞膜重新产生，并且不衰减地传播。施密特-尼尔森，p. 484。轴突的有髓神经切片不可激活，也不产生动作电位，信号被动地以电渗电位的形式传播。有规则间隔的无髓鞘补片，被称为郎飞结，产生动作电位来增强信号。这种类型的信号传播被称为跳跃式传导，它在信号传播速度和轴突直径之间提供了一个良好的折衷。轴突终末的去极化通常触发神经递质释放进入突触间隙。此外，在新皮层广泛存在的锥体神经元的树突中也记录到了反向传导的动作电位。这些都被认为在电峰时间相关突触可塑性中扮演着重要角色。

虽然动作电位是在可兴奋的膜片上局部产生的，但由此产生的电流可以触发相邻膜片上的动作电位，促成多米诺骨牌般的传播。与被动传播的电位(电紧张电位)不同，动作电位沿着可兴奋的细胞膜重新产生，并且不衰减地传播.<ref name="no_decrement" />。轴突的有髓鞘区域不可兴奋，不产生动作电位，信号被动地以电紧张电位的形式传播。规律性间隔的无髓鞘膜片，被称为郎飞结，产生动作电位来增强信号。这种类型的信号传播被称为跳跃式传导，它在信号传播速度和轴突直径之间提供了一个良好的折衷。轴突末梢的去极化通常触发神经递质释放进入突触间隙。此外，在新皮层广泛存在的锥体神经元的树突中也记录到了反向传播的动作电位.<ref name="backpropagation_in_pyramidal_cells" group="lower-alpha" />。这些都被认为在脉冲时间依赖的突触可塑性中起着重要作用。

In the [[Hodgkin–Huxley model|Hodgkin–Huxley membrane capacitance model]], the speed of transmission of an action potential was undefined and it was assumed that adjacent areas became depolarized due to released ion interference with neighbouring channels. Measurements of ion diffusion and radii have since shown this not to be possible.{{citation needed|date=November 2019}} Moreover, contradictory measurements of entropy changes and timing disputed the capacitance model as acting alone.{{citation needed|date=November 2019}} Alternatively, Gilbert Ling's adsorption hypothesis, posits that the membrane potential and action potential of a living cell is due to the adsorption of mobile ions onto adsorption sites of cells.<ref>{{cite journal | vauthors = Tamagawa H, Funatani M, Ikeda K | title = Ling's Adsorption Theory as a Mechanism of Membrane Potential Generation Observed in Both Living and Nonliving Systems | journal = Membranes | volume = 6 | issue = 1 | pages = 11 | date = January 2016 | pmid = 26821050 | pmc = 4812417 | doi = 10.3390/membranes6010011 | doi-access = free }}</ref>

In the [[Hodgkin–Huxley model|Hodgkin–Huxley membrane capacitance model]], the speed of transmission of an action potential was undefined and it was assumed that adjacent areas became depolarized due to released ion interference with neighbouring channels. Measurements of ion diffusion and radii have since shown this not to be possible.{{citation needed|date=November 2019}} Moreover, contradictory measurements of entropy changes and timing disputed the capacitance model as acting alone.{{citation needed|date=November 2019}} Alternatively, Gilbert Ling's adsorption hypothesis, posits that the membrane potential and action potential of a living cell is due to the adsorption of mobile ions onto adsorption sites of cells.<ref name=":8">{{cite journal | vauthors = Tamagawa H, Funatani M, Ikeda K | title = Ling's Adsorption Theory as a Mechanism of Membrane Potential Generation Observed in Both Living and Nonliving Systems | journal = Membranes | volume = 6 | issue = 1 | pages = 11 | date = January 2016 | pmid = 26821050 | pmc = 4812417 | doi = 10.3390/membranes6010011 | doi-access = free }}</ref>

在 Hodgkin-Huxley 膜电容模型中，动作电位的传递速度没有定义，假设邻近区域由于与邻近通道释放的离子干扰而去极化。离子扩散和半径的测量表明这是不可能的。此外，对熵变和时间的矛盾测量，质疑电容模型的独立作用。另外，Gilbert Ling 的吸附假说认为活细胞的膜电位和动作电位是由于活动离子吸附在细胞的吸附位点上。

在 Hodgkin-Huxley 膜电容模型中，动作电位的传输速度没有定义，假设邻近区域由于与邻近通道释放的离子干扰而去极化。离子扩散和半径的测量表明这是不可能的。此外，对熵变和时间的矛盾测量，质疑电容模型的独立作用。另外，Gilbert Ling 的吸附假说认为活细胞的膜电位和动作电位是由于活动离子吸附在细胞的吸附位点上.<ref name=":8" />。

=== Maturation of the electrical properties of the action potential ===

=== Maturation of the electrical properties of the action potential 动作电位的电性质的成熟 ===

A [[neuron]]'s ability to generate and propagate an action potential changes during [[Neural development|development]]. How much the [[membrane potential]] of a neuron changes as the result of a current impulse is a function of the membrane [[Input impedance|input resistance]]. As a cell grows, more [[Ion channel|channels]] are added to the membrane, causing a decrease in input resistance. A mature neuron also undergoes shorter changes in membrane potential in response to synaptic currents. Neurons from a ferret [[lateral geniculate nucleus]] have a longer [[time constant]] and larger [[voltage]] deflection at P0 than they do at P30.<ref name=":0">{{Cite book|title=Development of the nervous system|last1=Sanes|first1=Dan H.|last2=Reh|first2=Thomas A | name-list-style = vanc |date=2012-01-01|publisher=Elsevier Academic Press|isbn=9780080923208|pages=211–214|oclc=762720374|edition=Third}}</ref> One consequence of the decreasing action potential duration is that the fidelity of the signal can be preserved in response to high frequency stimulation. Immature neurons are more prone to synaptic depression than potentiation after high frequency stimulation.<ref name=":0" />

A [[neuron]]'s ability to generate and propagate an action potential changes during [[Neural development|development]]. How much the [[membrane potential]] of a neuron changes as the result of a current impulse is a function of the membrane [[Input impedance|input resistance]]. As a cell grows, more [[Ion channel|channels]] are added to the membrane, causing a decrease in input resistance. A mature neuron also undergoes shorter changes in membrane potential in response to synaptic currents. Neurons from a ferret [[lateral geniculate nucleus]] have a longer [[time constant]] and larger [[voltage]] deflection at P0 than they do at P30.<ref name=":0">{{Cite book|title=Development of the nervous system|last1=Sanes|first1=Dan H.|last2=Reh|first2=Thomas A | name-list-style = vanc |date=2012-01-01|publisher=Elsevier Academic Press|isbn=9780080923208|pages=211–214|oclc=762720374|edition=Third}}</ref> One consequence of the decreasing action potential duration is that the fidelity of the signal can be preserved in response to high frequency stimulation. Immature neurons are more prone to synaptic depression than potentiation after high frequency stimulation.<ref name=":0" />

= = = 动作电位电学性质的成熟 = = = 神经元在发育过程中产生和传播动作电位变化的能力。一个神经元在电流脉冲作用下的膜电位变化量是膜输入电阻的函数。随着细胞的增长，膜上增加了更多的通道，导致输入电阻减小。一个成熟的神经元在突触电流的作用下，在膜电位一分钟内也会发生较短的变化。雪貂外侧膝状核的神经元在 p 0时比在 p 30时有更长的时间常数和更大的电压偏转。动作电位持续时间减少的一个后果是，高频刺激可以保持信号的保真度。高频刺激后，未成熟神经元更容易发生突触抑制而非增强。

神经元产生和传播动作电位的能力在发育过程中发生变化。神经元在电流脉冲作用下的膜电位变化量是膜输入电阻的函数。随着细胞的增长，膜上增加了更多的通道，导致输入电阻减小。一个成熟的神经元在突触电流的作用下，在膜电位一分钟内也会发生较短的变化。雪貂外侧膝状核的神经元在 p 0时比在 p 30时有更长的时间常数和更大的电压偏转.<ref name=":0" /> 。动作电位持续时间减少的一个后果是，高频刺激可以保持信号的保真度。高频刺激后，未成熟神经元更容易发生突触抑制而非增强.<ref name=":0" /> 。

In the early development of many organisms, the action potential is actually initially carried by [[Calcium channel|calcium current]] rather than [[Sodium channel|sodium current]]. The [[Gating (electrophysiology)|opening and closing kinetics]] of calcium channels during development are slower than those of the voltage-gated sodium channels that will carry the action potential in the mature neurons. The longer opening times for the calcium channels can lead to action potentials that are considerably slower than those of mature neurons.<ref name=":0" /> [[Xenopus]] neurons initially have action potentials that take 60–90 ms. During development, this time decreases to 1 ms. There are two reasons for this drastic decrease. First, the [[Depolarization|inward current]] becomes primarily carried by sodium channels.<ref>{{Cite book|title=Calcium Channels: Their Properties, Functions, Regulation, and Clinical relevance|last=Partridge|first=Donald | name-list-style = vanc |publisher=CRC Press|year=1991|isbn=9780849388071|pages=138–142}}</ref> Second, the [[Voltage-gated potassium channel|delayed rectifier]], a [[potassium channel]] current, increases to 3.5 times its initial strength.<ref name=":0" />

In the early development of many organisms, the action potential is actually initially carried by [[Calcium channel|calcium current]] rather than [[Sodium channel|sodium current]]. The [[Gating (electrophysiology)|opening and closing kinetics]] of calcium channels during development are slower than those of the voltage-gated sodium channels that will carry the action potential in the mature neurons. The longer opening times for the calcium channels can lead to action potentials that are considerably slower than those of mature neurons.<ref name=":0" /> [[Xenopus]] neurons initially have action potentials that take 60–90 ms. During development, this time decreases to 1 ms. There are two reasons for this drastic decrease. First, the [[Depolarization|inward current]] becomes primarily carried by sodium channels.<ref name=":9">{{Cite book|title=Calcium Channels: Their Properties, Functions, Regulation, and Clinical relevance|last=Partridge|first=Donald | name-list-style = vanc |publisher=CRC Press|year=1991|isbn=9780849388071|pages=138–142}}</ref> Second, the [[Voltage-gated potassium channel|delayed rectifier]], a [[potassium channel]] current, increases to 3.5 times its initial strength.<ref name=":0" />

在许多生物体的早期发育过程中，动作电位实际上最初是由钙电流而不是钠电流携带的。发育过程中钙离子通道的开闭动力学比电压门控钠离子通道的开闭动力学要慢，而电压门控钠离子通道是成熟神经元的动作电位。钙离子通道的开放时间越长，动作电位的速度就会比成熟神经元慢得多。非洲爪蟾神经元最初的动作电位需要60-90毫秒。在发育过程中，这个时间减少到1毫秒。这种急剧下降有两个原因。首先，向内的电流主要由钠离子通道输送。其次，延迟整流器---- 一种钾离子通道电流---- 增加到最初强度的3.5倍。

在许多生物体的早期发育过程中，动作电位实际上最初是由钙电流而不是钠电流携带的。发育过程中钙离子通道的开闭动力学比电压门控钠离子通道的开闭动力学要慢，而电压门控钠离子通道是成熟神经元的动作电位。钙离子通道的开放时间越长，动作电位的速度就会比成熟神经元慢得多.<ref name=":0" /> 。非洲爪蟾神经元最初的动作电位需要60-90毫秒。在发育过程中，这个时间减少到1毫秒。这种急剧下降有两个原因。首先，向内的电流主要由钠离子通道输送.<ref name=":9" /> 。其次，延迟整流器---- 一种钾离子通道电流---- 增加到最初强度的3.5倍.<ref name=":0" /> 。

In order for the transition from a calcium-dependent action potential to a sodium-dependent action potential to proceed new channels must be added to the membrane. If Xenopus neurons are grown in an environment with [[Transcription (biology)|RNA synthesis]] or [[Translation (biology)|protein synthesis]] inhibitors that transition is prevented.<ref>{{Cite book|url=https://www.springer.com/us/book/9780306415500|title=Cellular and Molecular Biology of Neuronal Development {{!}} Ira Black {{!}} Springer|last=Black|first=Ira | name-list-style = vanc |publisher=Springer|year=1984|isbn=978-1-4613-2717-2|pages=103|language=en|url-status=live|archive-url=https://web.archive.org/web/20170717154858/http://www.springer.com/us/book/9780306415500|archive-date=17 July 2017|df=dmy-all}}</ref> Even the electrical activity of the cell itself may play a role in channel expression. If action potentials in Xenopus [[myocyte]]s are blocked, the typical increase in sodium and potassium current density is prevented or delayed.<ref>{{Cite book|title=Current Topics in Developmental Biology, Volume 39|last=Pedersen|first=Roger | name-list-style = vanc |publisher=Elsevier Academic Press|year=1998|isbn=9780080584621|url=https://archive.org/details/currenttopicsind0000unse_x6e1}}</ref>

In order for the transition from a calcium-dependent action potential to a sodium-dependent action potential to proceed new channels must be added to the membrane. If Xenopus neurons are grown in an environment with [[Transcription (biology)|RNA synthesis]] or [[Translation (biology)|protein synthesis]] inhibitors that transition is prevented.<ref name=":10">{{Cite book|url=https://www.springer.com/us/book/9780306415500|title=Cellular and Molecular Biology of Neuronal Development {{!}} Ira Black {{!}} Springer|last=Black|first=Ira | name-list-style = vanc |publisher=Springer|year=1984|isbn=978-1-4613-2717-2|pages=103|language=en|url-status=live|archive-url=https://web.archive.org/web/20170717154858/http://www.springer.com/us/book/9780306415500|archive-date=17 July 2017|df=dmy-all}}</ref> Even the electrical activity of the cell itself may play a role in channel expression. If action potentials in Xenopus [[myocyte]]s are blocked, the typical increase in sodium and potassium current density is prevented or delayed.<ref name=":11">{{Cite book|title=Current Topics in Developmental Biology, Volume 39|last=Pedersen|first=Roger | name-list-style = vanc |publisher=Elsevier Academic Press|year=1998|isbn=9780080584621|url=https://archive.org/details/currenttopicsind0000unse_x6e1}}</ref>

为了使依赖钙离子的动作电位转变为依赖钠离子的动作电位，膜上必须增加新的通道。如果非洲爪蟾神经元生长在有 RNA 合成抑制剂或蛋白质合成抑制剂的环境中，这种转变就被阻止了。甚至细胞本身的电活动也可能在通道表达中发挥作用。如果阻断非洲爪蟾心肌细胞的动作电位，钠和钾电流密度的典型增加就会被阻止或延迟。

为了使依赖钙离子的动作电位转变为依赖钠离子的动作电位，膜上必须增加新的通道。如果非洲爪蟾神经元生长在有 RNA 合成抑制剂或蛋白质合成抑制剂的环境中，这种转变就被阻止了.<ref name=":10" />。甚至细胞本身的电活动也可能在通道表达中发挥作用。如果阻断非洲爪蟾心肌细胞的动作电位，钠和钾电流密度的典型增加就会被阻止或延迟d.<ref name=":11" />。

This maturation of electrical properties is seen across species. Xenopus sodium and potassium currents increase drastically after a neuron goes through its final phase of [[mitosis]]. The sodium current density of rat [[Cerebral cortex|cortical neurons]] increases by 600% within the first two postnatal weeks.<ref name=":0" />

This maturation of electrical properties is seen across species. Xenopus sodium and potassium currents increase drastically after a neuron goes through its final phase of [[mitosis]]. The sodium current density of rat [[Cerebral cortex|cortical neurons]] increases by 600% within the first two postnatal weeks.<ref name=":0" />

这种电特性的成熟可以在不同物种间观察到。非洲爪蟾的钠和钾电流在神经元进入有丝分裂的最后阶段后急剧增加。大鼠大脑皮层神经元的钠电流密度在出生后第2周内增加了600% 。

这种电特性的成熟可以在不同物种间观察到。非洲爪蟾的钠和钾电流在神经元进入有丝分裂的最后阶段后急剧增加。大鼠大脑皮层神经元的钠电流密度在出生后第2周内增加了600% .<ref name=":0" />。

==Neurotransmission==

==Neurotransmission神经传递==

{{Main|Neurotransmission}}

===Anatomy of a neuron 神经元解剖===

{{Neuron map|Neuron}}

Several types of cells support an action potential, such as plant cells, muscle cells, and the specialized cells of the heart (in which occurs the [[cardiac action potential]]). However, the main excitable cell is the [[neuron]], which also has the simplest mechanism for the action potential.

Several types of cells support an action potential, such as plant cells, muscle cells, and the specialized cells of the heart (in which occurs the [[cardiac action potential]]). However, the main excitable cell is the [[neuron]], which also has the simplest mechanism for the action potential.

===Initiation===

===Initiation===

Before considering the propagation of action potentials along [[axon]]s and their termination at the synaptic knobs, it is helpful to consider the methods by which action potentials can be initiated at the [[axon hillock]]. The basic requirement is that the membrane voltage at the hillock be raised above the threshold for firing.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfn|Junge|1981|pp=89–90}}{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=49–50|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2pp=140–141|3a1=Schmidt-Nielsen|3y=1997|3pp=480-481}}{{sfn|Schmidt-Nielsen|1997|pp=483-484}} There are several ways in which this depolarization can occur.

Before considering the propagation of action potentials along [[axon]]s and their termination at the synaptic knobs, it is helpful to consider the methods by which action potentials can be initiated at the [[axon hillock]]. The basic requirement is that the membrane voltage at the hillock be raised above the threshold for firing.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfn|Junge|1981|pp=89–90}}{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=49–50|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2pp=140–141|3a1=Schmidt-Nielsen|3y=1997|3pp=480-481}}{{sfn|Schmidt-Nielsen|1997|pp=483-484}} There are several ways in which this depolarization can occur.

[[Image:SynapseSchematic en.svg|thumb|right|300px|When an action potential arrives at the end of the pre-synaptic axon (top), it causes the release of [[neurotransmitter]] molecules that open ion channels in the post-synaptic neuron (bottom). The combined [[excitatory postsynaptic potential|excitatory]] and [[inhibitory postsynaptic potential]]s of such inputs can begin a new action potential in the post-synaptic neuron.|链接=Special:FilePath/SynapseSchematic_en.svg]]

[[Image:SynapseSchematic en.svg|thumb|right|300px|When an action potential arrives at the end of the pre-synaptic axon (top), it causes the release of [[neurotransmitter]] molecules that open ion channels in the post-synaptic neuron (bottom). The combined [[excitatory postsynaptic potential|excitatory]] and [[inhibitory postsynaptic potential]]s of such inputs can begin a new action potential in the post-synaptic neuron.|链接=Special:FilePath/SynapseSchematic_en.svg]]

The [[amplitude]] of an action potential is independent of the amount of current that produced it. In other words, larger currents do not create larger action potentials. Therefore, action potentials are said to be [[All-or-none law|all-or-none]] signals, since either they occur fully or they do not occur at all.<ref name=" Sasaki " group=lower-alpha>Sasaki, T., Matsuki, N., Ikegaya, Y. 2011 Action-potential modulation during axonal conduction Science 331 (6017), pp. 599–601</ref><ref name="Aur" group=lower-alpha>{{cite journal | vauthors = Aur D, Connolly CI, Jog MS | title = Computing spike directivity with tetrodes | journal = Journal of Neuroscience Methods | volume = 149 | issue = 1 | pages = 57–63 | date = November 2005 | pmid = 15978667 | doi = 10.1016/j.jneumeth.2005.05.006 | s2cid = 34131910 }}</ref><ref name="Aur, Jog" group=lower-alpha>Aur D., Jog, MS., 2010 Neuroelectrodynamics: Understanding the brain language, IOS Press, 2010. {{DOI|10.3233/978-1-60750-473-3-i}}</ref> This is in contrast to [[receptor potential]]s, whose amplitudes are dependent on the intensity of a stimulus.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|pp=26–28}} In both cases, the [[frequency]] of action potentials is correlated with the intensity of a stimulus.

The [[amplitude]] of an action potential is independent of the amount of current that produced it. In other words, larger currents do not create larger action potentials. Therefore, action potentials are said to be [[All-or-none law|all-or-none]] signals, since either they occur fully or they do not occur at all.<ref name=" Sasaki " group=lower-alpha>Sasaki, T., Matsuki, N., Ikegaya, Y. 2011 Action-potential modulation during axonal conduction Science 331 (6017), pp. 599–601</ref><ref name="Aur" group=lower-alpha>{{cite journal | vauthors = Aur D, Connolly CI, Jog MS | title = Computing spike directivity with tetrodes | journal = Journal of Neuroscience Methods | volume = 149 | issue = 1 | pages = 57–63 | date = November 2005 | pmid = 15978667 | doi = 10.1016/j.jneumeth.2005.05.006 | s2cid = 34131910 }}</ref><ref name="Aur, Jog" group=lower-alpha>Aur D., Jog, MS., 2010 Neuroelectrodynamics: Understanding the brain language, IOS Press, 2010. {{DOI|10.3233/978-1-60750-473-3-i}}</ref> This is in contrast to [[receptor potential]]s, whose amplitudes are dependent on the intensity of a stimulus.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|pp=26–28}} In both cases, the [[frequency]] of action potentials is correlated with the intensity of a stimulus.

= = “全或无”原理 = = = 动作电位的振幅与产生动作电位的电流量无关。换句话说，更大的电流不会产生更大的动作电位。因此，动作电位被称为全或无信号，因为它们要么完全发生，要么根本不发生。佐佐木，t. ，松木，纽约，Ikegaya，y。2011轴突传导期间的动作电位调制。599-601Aur d. ，Jog，ms，2010《神经电动力学: 理解大脑语言》 ，IOS 出版社，2010。这与受体电位相反，受体电位的振幅取决于刺激的强度。在这两种情况下，动作电位的频率都与刺激的强度相关。

= = “全或无”原理 = = = 动作电位的振幅与产生动作电位的电流量无关。换句话说，更大的电流不会产生更大的动作电位。因此，动作电位被称为全或无信号，因为它们要么完全发生，要么根本不发生 all.<ref name="Sasaki" group="lower-alpha" /><ref name="Aur" group="lower-alpha" /><ref name="Aur, Jog" group="lower-alpha" /> 。佐佐木，t. ，松木，纽约，Ikegaya，y。2011轴突传导期间的动作电位调制。599-601Aur d. ，Jog，ms，2010《神经电动力学: 理解大脑语言》 ，IOS 出版社，2010。这与受体电位相反，受体电位的振幅取决于刺激的强度。在这两种情况下，动作电位的频率都与刺激的强度相关。

===Sensory neurons===

===Sensory neurons===

In sensory neurons, action potentials result from an external stimulus. However, some excitable cells require no such stimulus to fire: They spontaneously depolarize their axon hillock and fire action potentials at a regular rate, like an internal clock.{{sfn|Junge|1981|pp=115–132}} The voltage traces of such cells are known as [[pacemaker potential]]s.{{sfn|Bullock|Orkand|Grinnell|1977|pp=152–153}} The [[cardiac pacemaker]] cells of the [[sinoatrial node]] in the [[heart]] provide a good example.<ref name="noble_1960" group=lower-alpha >{{cite journal | vauthors = Noble D | title = Cardiac action and pacemaker potentials based on the Hodgkin-Huxley equations | journal = Nature | volume = 188 | issue = 4749 | pages = 495–7 | date = November 1960 | pmid = 13729365 | doi = 10.1038/188495b0 | bibcode = 1960Natur.188..495N | s2cid = 4147174 }}</ref> Although such pacemaker potentials have a [[neural oscillation|natural rhythm]], it can be adjusted by external stimuli; for instance, [[heart rate]] can be altered by pharmaceuticals as well as signals from the [[sympathetic nervous system|sympathetic]] and [[parasympathetic nervous system|parasympathetic]] nerves.{{sfn|Bullock|Orkand|Grinnell|1977|pp=444–445}} The external stimuli do not cause the cell's repetitive firing, but merely alter its timing.{{sfn|Bullock|Orkand|Grinnell|1977|pp=152–153}} In some cases, the regulation of frequency can be more complex, leading to patterns of action potentials, such as [[bursting]].

In sensory neurons, action potentials result from an external stimulus. However, some excitable cells require no such stimulus to fire: They spontaneously depolarize their axon hillock and fire action potentials at a regular rate, like an internal clock.{{sfn|Junge|1981|pp=115–132}} The voltage traces of such cells are known as [[pacemaker potential]]s.{{sfn|Bullock|Orkand|Grinnell|1977|pp=152–153}} The [[cardiac pacemaker]] cells of the [[sinoatrial node]] in the [[heart]] provide a good example.<ref name="noble_1960" group=lower-alpha >{{cite journal | vauthors = Noble D | title = Cardiac action and pacemaker potentials based on the Hodgkin-Huxley equations | journal = Nature | volume = 188 | issue = 4749 | pages = 495–7 | date = November 1960 | pmid = 13729365 | doi = 10.1038/188495b0 | bibcode = 1960Natur.188..495N | s2cid = 4147174 }}</ref> Although such pacemaker potentials have a [[neural oscillation|natural rhythm]], it can be adjusted by external stimuli; for instance, [[heart rate]] can be altered by pharmaceuticals as well as signals from the [[sympathetic nervous system|sympathetic]] and [[parasympathetic nervous system|parasympathetic]] nerves.{{sfn|Bullock|Orkand|Grinnell|1977|pp=444–445}} The external stimuli do not cause the cell's repetitive firing, but merely alter its timing.{{sfn|Bullock|Orkand|Grinnell|1977|pp=152–153}} In some cases, the regulation of frequency can be more complex, leading to patterns of action potentials, such as [[bursting]].

在感觉神经元中，动作电位来自外部刺激。然而，一些易激活的细胞不需要这样的刺激就可以激活: 它们自发地使轴突突起去极化，并以一个规律的速率激活动作电位，就像一个内部的时钟。这种细胞的电压痕迹称为起搏电位。心脏窦房结的心律调节器细胞就是一个很好的例子。虽然这种起搏器电位具有自然节律，但它可以通过外部刺激进行调节; 例如，药物以及交感神经和副交感神经发出的信号可以改变心率。外部刺激不会引起细胞的反复放电，只是改变了它的放电时间。在某些情况下，频率的调节可能更加复杂，导致动作电位的模式，如爆发。

在感觉神经元中，动作电位来自外部刺激。然而，一些易激活的细胞不需要这样的刺激就可以激活: 它们自发地使轴突突起去极化，并以一个规律的速率激活动作电位，就像一个内部的时钟。这种细胞的电压痕迹称为起搏电位。心脏窦房结的心律调节器细胞就是一个很好的例子le.<ref name="noble_1960" group="lower-alpha" />。虽然这种起搏器电位具有自然节律，但它可以通过外部刺激进行调节; 例如，药物以及交感神经和副交感神经发出的信号可以改变心率。外部刺激不会引起细胞的反复放电，只是改变了它的放电时间。在某些情况下，频率的调节可能更加复杂，导致动作电位的模式，如爆发。

==Phases==

==Phases==

The course of the action potential is determined by two coupled effects.{{sfn|Stevens|1966|pp=127–128}} First, voltage-sensitive ion channels open and close in response to changes in the [[membrane potential|membrane voltage]] ''V_m''. This changes the membrane's permeability to those ions.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|pp=61–65}} Second, according to the [[Goldman equation]], this change in permeability changes the equilibrium potential ''E_m'', and, thus, the membrane voltage ''V_m''.<ref name="goldman_1943" group="lower-alpha">{{cite journal | vauthors = Goldman DE | title = Potential, Impedance, and Rectification in Membranes | journal = The Journal of General Physiology | volume = 27 | issue = 1 | pages = 37–60 | date = September 1943 | pmid = 19873371 | pmc = 2142582 | doi = 10.1085/jgp.27.1.37 }}</ref> Thus, the membrane potential affects the permeability, which then further affects the membrane potential. This sets up the possibility for [[positive feedback]], which is a key part of the rising phase of the action potential.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=48–49|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2p=141|3a1=Schmidt-Nielsen|3y=1997|3p=483|4a1=Junge|4y=1981|4p=89}} A complicating factor is that a single ion channel may have multiple internal "gates" that respond to changes in ''V_m'' in opposite ways, or at different rates.{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=64–74|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2pp=149–150|3a1=Junge|3y=1981|3pp=84–85|4a1=Stevens|4y=1966|4pp=152–158}}<ref name="hodgkin_1952" group="lower-alpha">{{cite journal | vauthors = Hodgkin AL, Huxley AF, Katz B | title = Measurement of current-voltage relations in the membrane of the giant axon of Loligo | journal = The Journal of Physiology | volume = 116 | issue = 4 | pages = 424–48 | date = April 1952 | pmid = 14946712 | pmc = 1392219 | doi = 10.1113/jphysiol.1952.sp004716 | author-link1 = Alan Lloyd Hodgkin | author-link3 = Bernard Katz }}<br />* {{cite journal | vauthors = Hodgkin AL, Huxley AF | title = Currents carried by sodium and potassium ions through the membrane of the giant axon of Loligo | journal = The Journal of Physiology | volume = 116 | issue = 4 | pages = 449–72 | date = April 1952 | pmid = 14946713 | pmc = 1392213 | doi = 10.1113/jphysiol.1952.sp004717 | author-link1 = Alan Lloyd Hodgkin }}<br />* {{cite journal | vauthors = Hodgkin AL, Huxley AF | title = The components of membrane conductance in the giant axon of Loligo | journal = The Journal of Physiology | volume = 116 | issue = 4 | pages = 473–96 | date = April 1952 | pmid = 14946714 | pmc = 1392209 | doi = 10.1113/jphysiol.1952.sp004718 | author-link1 = Alan Lloyd Hodgkin }}<br />* {{cite journal | vauthors = Hodgkin AL, Huxley AF | title = The dual effect of membrane potential on sodium conductance in the giant axon of Loligo | journal = The Journal of Physiology | volume = 116 | issue = 4 | pages = 497–506 | date = April 1952 | pmid = 14946715 | pmc = 1392212 | doi = 10.1113/jphysiol.1952.sp004719 | author-link1 = Alan Lloyd Hodgkin }}<br />* {{cite journal | vauthors = Hodgkin AL, Huxley AF | title = A quantitative description of membrane current and its application to conduction and excitation in nerve | journal = The Journal of Physiology | volume = 117 | issue = 4 | pages = 500–44 | date = August 1952 | pmid = 12991237 | pmc = 1392413 | doi = 10.1113/jphysiol.1952.sp004764 | author-link1 = Alan Lloyd Hodgkin }}</ref> For example, although raising ''V_m'' ''opens'' most gates in the voltage-sensitive sodium channel, it also ''closes'' the channel's "inactivation gate", albeit more slowly.{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1p=47|2a1=Purves|2a2=Augustine|2a3=Fitzpatrick|2a4=Hall|2y=2008|2p=65|3a1=Bullock|3a2=Orkand|3a3=Grinnell|3y=1977|3pp=147–148|4a1=Stevens|4y=1966|4p=128}} Hence, when ''V_m'' is raised suddenly, the sodium channels open initially, but then close due to the slower inactivation.

The course of the action potential is determined by two coupled effects.{{sfn|Stevens|1966|pp=127–128}} First, voltage-sensitive ion channels open and close in response to changes in the [[membrane potential|membrane voltage]] ''V_m''. This changes the membrane's permeability to those ions.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|pp=61–65}} Second, according to the [[Goldman equation]], this change in permeability changes the equilibrium potential ''E_m'', and, thus, the membrane voltage ''V_m''.<ref name="goldman_1943" group="lower-alpha">{{cite journal | vauthors = Goldman DE | title = Potential, Impedance, and Rectification in Membranes | journal = The Journal of General Physiology | volume = 27 | issue = 1 | pages = 37–60 | date = September 1943 | pmid = 19873371 | pmc = 2142582 | doi = 10.1085/jgp.27.1.37 }}</ref> Thus, the membrane potential affects the permeability, which then further affects the membrane potential. This sets up the possibility for [[positive feedback]], which is a key part of the rising phase of the action potential.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=48–49|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2p=141|3a1=Schmidt-Nielsen|3y=1997|3p=483|4a1=Junge|4y=1981|4p=89}} A complicating factor is that a single ion channel may have multiple internal "gates" that respond to changes in ''V_m'' in opposite ways, or at different rates.{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=64–74|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2pp=149–150|3a1=Junge|3y=1981|3pp=84–85|4a1=Stevens|4y=1966|4pp=152–158}}<ref name="hodgkin_1952" group="lower-alpha">{{cite journal | vauthors = Hodgkin AL, Huxley AF, Katz B | title = Measurement of current-voltage relations in the membrane of the giant axon of Loligo | journal = The Journal of Physiology | volume = 116 | issue = 4 | pages = 424–48 | date = April 1952 | pmid = 14946712 | pmc = 1392219 | doi = 10.1113/jphysiol.1952.sp004716 | author-link1 = Alan Lloyd Hodgkin | author-link3 = Bernard Katz }}<br />* {{cite journal | vauthors = Hodgkin AL, Huxley AF | title = Currents carried by sodium and potassium ions through the membrane of the giant axon of Loligo | journal = The Journal of Physiology | volume = 116 | issue = 4 | pages = 449–72 | date = April 1952 | pmid = 14946713 | pmc = 1392213 | doi = 10.1113/jphysiol.1952.sp004717 | author-link1 = Alan Lloyd Hodgkin }}<br />* {{cite journal | vauthors = Hodgkin AL, Huxley AF | title = The components of membrane conductance in the giant axon of Loligo | journal = The Journal of Physiology | volume = 116 | issue = 4 | pages = 473–96 | date = April 1952 | pmid = 14946714 | pmc = 1392209 | doi = 10.1113/jphysiol.1952.sp004718 | author-link1 = Alan Lloyd Hodgkin }}<br />* {{cite journal | vauthors = Hodgkin AL, Huxley AF | title = The dual effect of membrane potential on sodium conductance in the giant axon of Loligo | journal = The Journal of Physiology | volume = 116 | issue = 4 | pages = 497–506 | date = April 1952 | pmid = 14946715 | pmc = 1392212 | doi = 10.1113/jphysiol.1952.sp004719 | author-link1 = Alan Lloyd Hodgkin }}<br />* {{cite journal | vauthors = Hodgkin AL, Huxley AF | title = A quantitative description of membrane current and its application to conduction and excitation in nerve | journal = The Journal of Physiology | volume = 117 | issue = 4 | pages = 500–44 | date = August 1952 | pmid = 12991237 | pmc = 1392413 | doi = 10.1113/jphysiol.1952.sp004764 | author-link1 = Alan Lloyd Hodgkin }}</ref> For example, although raising ''V_m'' ''opens'' most gates in the voltage-sensitive sodium channel, it also ''closes'' the channel's "inactivation gate", albeit more slowly.{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1p=47|2a1=Purves|2a2=Augustine|2a3=Fitzpatrick|2a4=Hall|2y=2008|2p=65|3a1=Bullock|3a2=Orkand|3a3=Grinnell|3y=1977|3pp=147–148|4a1=Stevens|4y=1966|4p=128}} Hence, when ''V_m'' is raised suddenly, the sodium channels open initially, but then close due to the slower inactivation.

动作电位的过程是由两个耦合效应决定的。首先，电压敏感离子通道的开启和关闭是为了响应膜电位的变化。这改变了膜对这些离子的渗透性。其次，根据戈德曼方程的研究，这种渗透率的变化改变了平衡电位 Em，从而改变了膜电位。因此，膜电位影响渗透性，进而进一步影响膜电位。这就为正反馈提供了可能性，而正反馈是动作电位上升阶段的关键部分。一个复杂的因素是，单个离子通道可能有多个内部“门”，以相反的方式或不同的速率响应 Vm 中的变化。例如，尽管提高 Vm 可以打开电压敏感钠通道中的大多数门，但它也可以关闭通道的“失活门”，尽管速度更慢。因此，当 Vm 突然升高时，钠离子通道开始打开，但随后由于较慢的失活而关闭。

动作电位的过程是由两个耦合效应决定的。首先，电压敏感离子通道的开启和关闭是为了响应膜电位的变化。这改变了膜对这些离子的渗透性。其次，根据戈德曼方程的研究，这种渗透率的变化改变了平衡电位 Em，从而改变了膜电位.<ref name="goldman_1943" group="lower-alpha" /> T。因此，膜电位影响渗透性，进而进一步影响膜电位。这就为正反馈提供了可能性，而正反馈是动作电位上升阶段的关键部分。一个复杂的因素是，单个离子通道可能有多个内部“门”，以相反的方式或不同的速率响应 Vm 中的变化.{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=64–74|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2pp=149–150|3a1=Junge|3y=1981|3pp=84–85|4a1=Stevens|4y=1966|4pp=152–158}}<ref name="hodgkin_1952" group="lower-alpha" /> F<ref name="hodgkin_1952" group="lower-alpha" />。例如，尽管提高 Vm 可以打开电压敏感钠通道中的大多数门，但它也可以关闭通道的“失活门”，尽管速度更慢。因此，当 Vm 突然升高时，钠离子通道开始打开，但随后由于较慢的失活而关闭。

The voltages and currents of the action potential in all of its phases were modeled accurately by [[Alan Lloyd Hodgkin]] and [[Andrew Huxley]] in 1952,<ref name="hodgkin_1952" group=lower-alpha /> for which they were awarded the [[Nobel Prize in Physiology or Medicine]] in 1963.<ref name="Nobel_1963" group=lower-Greek>{{cite press release | url = http://nobelprize.org/nobel_prizes/medicine/laureates/1963/index.html | title = The Nobel Prize in Physiology or Medicine 1963 | publisher = The Royal Swedish Academy of Science | year = 1963 | access-date = 2010-02-21 | url-status = live | archive-url = https://web.archive.org/web/20070716195411/http://nobelprize.org/nobel_prizes/medicine/laureates/1963/index.html | archive-date = 16 July 2007 | df = dmy-all }}</ref> However, [[Hodgkin–Huxley model|their model]] considers only two types of voltage-sensitive ion channels, and makes several assumptions about them, e.g., that their internal gates open and close independently of one another. In reality, there are many types of ion channels,<ref name="goldin_2007">Goldin, AL in {{harvnb|Waxman|2007|loc=''Neuronal Channels and Receptors'', pp. 43–58.}}</ref> and they do not always open and close independently.<ref group=lower-alpha>{{cite journal | vauthors = Naundorf B, Wolf F, Volgushev M | title = Unique features of action potential initiation in cortical neurons | journal = Nature | volume = 440 | issue = 7087 | pages = 1060–3 | date = April 2006 | pmid = 16625198 | doi = 10.1038/nature04610 | url = http://www.volgushev.uconn.edu/DownLoads/Naundorf_Nature2006v440p1060_Suppl_3_CoopModel.pdf | df = dmy-all | bibcode = 2006Natur.440.1060N | s2cid = 1328840 }}</ref>

The voltages and currents of the action potential in all of its phases were modeled accurately by [[Alan Lloyd Hodgkin]] and [[Andrew Huxley]] in 1952,<ref name="hodgkin_1952" group=lower-alpha /> for which they were awarded the [[Nobel Prize in Physiology or Medicine]] in 1963.<ref name="Nobel_1963" group=lower-Greek>{{cite press release | url = http://nobelprize.org/nobel_prizes/medicine/laureates/1963/index.html | title = The Nobel Prize in Physiology or Medicine 1963 | publisher = The Royal Swedish Academy of Science | year = 1963 | access-date = 2010-02-21 | url-status = live | archive-url = https://web.archive.org/web/20070716195411/http://nobelprize.org/nobel_prizes/medicine/laureates/1963/index.html | archive-date = 16 July 2007 | df = dmy-all }}</ref> However, [[Hodgkin–Huxley model|their model]] considers only two types of voltage-sensitive ion channels, and makes several assumptions about them, e.g., that their internal gates open and close independently of one another. In reality, there are many types of ion channels,<ref name="goldin_2007">Goldin, AL in {{harvnb|Waxman|2007|loc=''Neuronal Channels and Receptors'', pp. 43–58.}}</ref> and they do not always open and close independently.<ref group="lower-alpha" name=":0">{{cite journal | vauthors = Naundorf B, Wolf F, Volgushev M | title = Unique features of action potential initiation in cortical neurons | journal = Nature | volume = 440 | issue = 7087 | pages = 1060–3 | date = April 2006 | pmid = 16625198 | doi = 10.1038/nature04610 | url = http://www.volgushev.uconn.edu/DownLoads/Naundorf_Nature2006v440p1060_Suppl_3_CoopModel.pdf | df = dmy-all | bibcode = 2006Natur.440.1060N | s2cid = 1328840 }}</ref>

艾伦·劳埃德·霍奇金和 Andrew Huxley 在1952年精确地模拟了动作电位各个阶段的电压和电流，并因此在1963年获得了诺贝尔生理学或医学奖动作电位奖。然而，他们的模型只考虑了两种类型的电压敏感离子通道，并对它们做出了几个假设，例如，它们的内部门的开启和关闭是相互独立的。实际上，离子通道有很多种类型，戈尔丁通道和铝通道，它们并不总是独立开启和关闭的。

艾伦·劳埃德·霍奇金和 Andrew Huxley 在1952年精确地模拟了动作电位各个阶段的电压和电流,<ref name="hodgkin_1952" group="lower-alpha" /> f。，并因此在1963年获得了诺贝尔生理学或医学奖动作电位奖523.<ref name="Nobel_1963" group="lower-Greek" /> 然而，他们的模型只考虑了两种类型的电压敏感离子通道，并对它们做出了几个假设，例如，它们的内部门的开启和关闭是相互独立的。实际上，离子通道有很多种类型，戈尔丁通道和铝通道s,<ref name="goldin_2007" /> a，它们并不总是独立开启和关闭的y.<ref name=":0" group="lower-alpha" />。

===Stimulation and rising phase===

===Stimulation and rising phase===

{{Main|Nerve conduction velocity}} <!-- note: factually not a main article, but a stub in need of expansion; perhaps the material below should simply be moved there and a summary left in its place -->

{{Main|Nerve conduction velocity}} <!-- note: factually not a main article, but a stub in need of expansion; perhaps the material below should simply be moved there and a summary left in its place -->

The action potential generated at the axon hillock propagates as a wave along the axon.{{sfn|Bullock|Orkand|Grinnell|1977|pp=160–164}} The currents flowing inwards at a point on the axon during an action potential spread out along the axon, and depolarize the adjacent sections of its membrane. If sufficiently strong, this depolarization provokes a similar action potential at the neighboring membrane patches. This basic mechanism was demonstrated by [[Alan Lloyd Hodgkin]] in 1937. After crushing or cooling nerve segments and thus blocking the action potentials, he showed that an action potential arriving on one side of the block could provoke another action potential on the other, provided that the blocked segment was sufficiently short.<ref group=lower-alpha>{{cite journal | vauthors = Hodgkin AL | title = Evidence for electrical transmission in nerve: Part I | journal = The Journal of Physiology | volume = 90 | issue = 2 | pages = 183–210 | date = July 1937 | pmid = 16994885 | pmc = 1395060 | doi = 10.1113/jphysiol.1937.sp003507 | author-link = Alan Lloyd Hodgkin }}<br />* {{cite journal | vauthors = Hodgkin AL | title = Evidence for electrical transmission in nerve: Part II | journal = The Journal of Physiology | volume = 90 | issue = 2 | pages = 211–32 | date = July 1937 | pmid = 16994886 | pmc = 1395062 | doi = 10.1113/jphysiol.1937.sp003508 | author-link = Alan Lloyd Hodgkin }}</ref>

The action potential generated at the axon hillock propagates as a wave along the axon.{{sfn|Bullock|Orkand|Grinnell|1977|pp=160–164}} The currents flowing inwards at a point on the axon during an action potential spread out along the axon, and depolarize the adjacent sections of its membrane. If sufficiently strong, this depolarization provokes a similar action potential at the neighboring membrane patches. This basic mechanism was demonstrated by [[Alan Lloyd Hodgkin]] in 1937. After crushing or cooling nerve segments and thus blocking the action potentials, he showed that an action potential arriving on one side of the block could provoke another action potential on the other, provided that the blocked segment was sufficiently short.<ref group="lower-alpha" name=":1">{{cite journal | vauthors = Hodgkin AL | title = Evidence for electrical transmission in nerve: Part I | journal = The Journal of Physiology | volume = 90 | issue = 2 | pages = 183–210 | date = July 1937 | pmid = 16994885 | pmc = 1395060 | doi = 10.1113/jphysiol.1937.sp003507 | author-link = Alan Lloyd Hodgkin }}<br />* {{cite journal | vauthors = Hodgkin AL | title = Evidence for electrical transmission in nerve: Part II | journal = The Journal of Physiology | volume = 90 | issue = 2 | pages = 211–32 | date = July 1937 | pmid = 16994886 | pmc = 1395062 | doi = 10.1113/jphysiol.1937.sp003508 | author-link = Alan Lloyd Hodgkin }}</ref>

<nowiki>*</nowiki>  

<nowiki>*</nowiki>  

轴突柄处产生的动作电位沿轴突传播。当动作电位沿轴突扩散时，电流在轴突上的某一点向内流动，并使其膜的相邻部分去极化。如果足够强的话，这种去极化会在相邻的膜片上激发类似的动作电位。这一基本机制在1937年由艾伦·劳埃德·霍奇金证明。在挤压或冷却神经节段，从而阻断动作电位后，他表明，动作电位到达阻滞的一侧可以激发另一侧的动作电位，只要阻滞的节段足够短。< br/> *  

轴突柄处产生的动作电位沿轴突传播。当动作电位沿轴突扩散时，电流在轴突上的某一点向内流动，并使其膜的相邻部分去极化。如果足够强的话，这种去极化会在相邻的膜片上激发类似的动作电位。这一基本机制在1937年由艾伦·劳埃德·霍奇金证明。在挤压或冷却神经节段，从而阻断动作电位后，他表明，动作电位到达阻滞的一侧可以激发另一侧的动作电位，只要阻滞的节段足够短。rt.<ref name=":1" group="lower-alpha" />< br/> *  

Once an action potential has occurred at a patch of membrane, the membrane patch needs time to recover before it can fire again. At the molecular level, this ''absolute refractory period'' corresponds to the time required for the voltage-activated sodium channels to recover from inactivation, i.e., to return to their closed state.{{sfn|Stevens|1966|pp=19–20}} There are many types of voltage-activated potassium channels in neurons. Some of them inactivate fast (A-type currents) and some of them inactivate slowly or not inactivate at all; this variability guarantees that there will be always an available source of current for repolarization, even if some of the potassium channels are inactivated because of preceding depolarization. On the other hand, all neuronal voltage-activated sodium channels inactivate within several milliseconds during strong depolarization, thus making following depolarization impossible until a substantial fraction of sodium channels have returned to their closed state. Although it limits the frequency of firing,{{sfn|Stevens|1966|pp=21–23}} the absolute refractory period ensures that the action potential moves in only one direction along an axon.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|p=56}} The currents flowing in due to an action potential spread out in both directions along the axon.{{sfn|Bullock|Orkand|Grinnell|1977|pp=161–164}} However, only the unfired part of the axon can respond with an action potential; the part that has just fired is unresponsive until the action potential is safely out of range and cannot restimulate that part. In the usual [[orthodromic conduction]], the action potential propagates from the axon hillock towards the synaptic knobs (the axonal termini); propagation in the opposite direction—known as [[antidromic conduction]]—is very rare.{{sfn|Bullock|Orkand|Grinnell|1977|p=509}} However, if a laboratory axon is stimulated in its middle, both halves of the axon are "fresh", i.e., unfired; then two action potentials will be generated, one traveling towards the axon hillock and the other traveling towards the synaptic knobs.

Once an action potential has occurred at a patch of membrane, the membrane patch needs time to recover before it can fire again. At the molecular level, this ''absolute refractory period'' corresponds to the time required for the voltage-activated sodium channels to recover from inactivation, i.e., to return to their closed state.{{sfn|Stevens|1966|pp=19–20}} There are many types of voltage-activated potassium channels in neurons. Some of them inactivate fast (A-type currents) and some of them inactivate slowly or not inactivate at all; this variability guarantees that there will be always an available source of current for repolarization, even if some of the potassium channels are inactivated because of preceding depolarization. On the other hand, all neuronal voltage-activated sodium channels inactivate within several milliseconds during strong depolarization, thus making following depolarization impossible until a substantial fraction of sodium channels have returned to their closed state. Although it limits the frequency of firing,{{sfn|Stevens|1966|pp=21–23}} the absolute refractory period ensures that the action potential moves in only one direction along an axon.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|p=56}} The currents flowing in due to an action potential spread out in both directions along the axon.{{sfn|Bullock|Orkand|Grinnell|1977|pp=161–164}} However, only the unfired part of the axon can respond with an action potential; the part that has just fired is unresponsive until the action potential is safely out of range and cannot restimulate that part. In the usual [[orthodromic conduction]], the action potential propagates from the axon hillock towards the synaptic knobs (the axonal termini); propagation in the opposite direction—known as [[antidromic conduction]]—is very rare.{{sfn|Bullock|Orkand|Grinnell|1977|p=509}} However, if a laboratory axon is stimulated in its middle, both halves of the axon are "fresh", i.e., unfired; then two action potentials will be generated, one traveling towards the axon hillock and the other traveling towards the synaptic knobs.

{{Main|Myelination|Saltatory conduction}}

{{Main|Myelination|Saltatory conduction}}

In order to enable fast and efficient transduction of electrical signals in the nervous system, certain neuronal axons are covered with [[myelin]] sheaths. Myelin is a multilamellar membrane that enwraps the axon in segments separated by intervals known as [[nodes of Ranvier]]. It is produced by specialized cells: [[Schwann cell]]s exclusively in the [[peripheral nervous system]], and [[oligodendrocyte]]s exclusively in the [[central nervous system]]. Myelin sheath reduces membrane capacitance and increases membrane resistance in the inter-node intervals, thus allowing a fast, saltatory movement of action potentials from node to node.<ref name=Zalc group=lower-alpha>{{cite journal | vauthors = Zalc B | title = The acquisition of myelin: a success story | journal = Novartis Foundation Symposium | volume = 276 | pages = 15–21; discussion 21–5, 54–7, 275–81 | year = 2006 | pmid = 16805421 | doi = 10.1002/9780470032244.ch3 | isbn = 978-0-470-03224-4 | series = Novartis Foundation Symposia }}</ref><ref name="S. Poliak & E. Peles" group=lower-alpha>{{cite journal | vauthors = Poliak S, Peles E | title = The local differentiation of myelinated axons at nodes of Ranvier | journal = Nature Reviews. Neuroscience | volume = 4 | issue = 12 | pages = 968–80 | date = December 2003 | pmid = 14682359 | doi = 10.1038/nrn1253 | s2cid = 14720760 }}</ref><ref group=lower-alpha>{{cite journal | vauthors = Simons M, Trotter J | title = Wrapping it up: the cell biology of myelination | journal = Current Opinion in Neurobiology | volume = 17 | issue = 5 | pages = 533–40 | date = October 2007 | pmid = 17923405 | doi = 10.1016/j.conb.2007.08.003 | s2cid = 45470194 }}</ref> Myelination is found mainly in [[vertebrate]]s, but an analogous system has been discovered in a few invertebrates, such as some species of [[shrimp]].<ref group=lower-alpha>{{cite journal | vauthors = Xu K, Terakawa S | title = Fenestration nodes and the wide submyelinic space form the basis for the unusually fast impulse conduction of shrimp myelinated axons | journal = The Journal of Experimental Biology | volume = 202 | issue = Pt 15 | pages = 1979–89 | date = August 1999 | doi = 10.1242/jeb.202.15.1979 | pmid = 10395528 | url = http://jeb.biologists.org/cgi/pmidlookup?view=long&pmid=10395528 }}</ref> Not all neurons in vertebrates are myelinated; for example, axons of the neurons comprising the autonomous nervous system are not, in general, myelinated.

In order to enable fast and efficient transduction of electrical signals in the nervous system, certain neuronal axons are covered with [[myelin]] sheaths. Myelin is a multilamellar membrane that enwraps the axon in segments separated by intervals known as [[nodes of Ranvier]]. It is produced by specialized cells: [[Schwann cell]]s exclusively in the [[peripheral nervous system]], and [[oligodendrocyte]]s exclusively in the [[central nervous system]]. Myelin sheath reduces membrane capacitance and increases membrane resistance in the inter-node intervals, thus allowing a fast, saltatory movement of action potentials from node to node.<ref name=Zalc group=lower-alpha>{{cite journal | vauthors = Zalc B | title = The acquisition of myelin: a success story | journal = Novartis Foundation Symposium | volume = 276 | pages = 15–21; discussion 21–5, 54–7, 275–81 | year = 2006 | pmid = 16805421 | doi = 10.1002/9780470032244.ch3 | isbn = 978-0-470-03224-4 | series = Novartis Foundation Symposia }}</ref><ref name="S. Poliak & E. Peles" group=lower-alpha>{{cite journal | vauthors = Poliak S, Peles E | title = The local differentiation of myelinated axons at nodes of Ranvier | journal = Nature Reviews. Neuroscience | volume = 4 | issue = 12 | pages = 968–80 | date = December 2003 | pmid = 14682359 | doi = 10.1038/nrn1253 | s2cid = 14720760 }}</ref><ref group="lower-alpha" name=":2">{{cite journal | vauthors = Simons M, Trotter J | title = Wrapping it up: the cell biology of myelination | journal = Current Opinion in Neurobiology | volume = 17 | issue = 5 | pages = 533–40 | date = October 2007 | pmid = 17923405 | doi = 10.1016/j.conb.2007.08.003 | s2cid = 45470194 }}</ref> Myelination is found mainly in [[vertebrate]]s, but an analogous system has been discovered in a few invertebrates, such as some species of [[shrimp]].<ref group="lower-alpha" name=":3">{{cite journal | vauthors = Xu K, Terakawa S | title = Fenestration nodes and the wide submyelinic space form the basis for the unusually fast impulse conduction of shrimp myelinated axons | journal = The Journal of Experimental Biology | volume = 202 | issue = Pt 15 | pages = 1979–89 | date = August 1999 | doi = 10.1242/jeb.202.15.1979 | pmid = 10395528 | url = http://jeb.biologists.org/cgi/pmidlookup?view=long&pmid=10395528 }}</ref> Not all neurons in vertebrates are myelinated; for example, axons of the neurons comprising the autonomous nervous system are not, in general, myelinated.

为了在神经系统中快速有效地传递电信号，某些神经元的轴突上覆盖着髓鞘。髓鞘是一种多层膜，它将轴突包裹在一段段中，这段段间隔被称为郎飞结。它是由专门的细胞产生的: 施万细胞专门在周围神经系统，少突胶质细胞专门在中枢神经系统。髓鞘减少膜电容和增加膜电阻在节间间隔，从而允许快速，跳跃性的动作电位从一个节点到另一个节点。髓鞘形成主要存在于脊椎动物中，但是在一些无脊椎动物中也发现了类似的系统，比如某些种类的虾。脊椎动物中并不是所有的神经元都是有髓神经元; 例如，组成自主神经系统的神经元的轴突一般都不是有髓神经元。

为了在神经系统中快速有效地传递电信号，某些神经元的轴突上覆盖着髓鞘。髓鞘是一种多层膜，它将轴突包裹在一段段中，这段段间隔被称为郎飞结。它是由专门的细胞产生的: 施万细胞专门在周围神经系统，少突胶质细胞专门在中枢神经系统。髓鞘减少膜电容和增加膜电阻在节间间隔，从而允许快速，跳跃性的动作电位从一个节点到另一个节点e.<ref name="Zalc" group="lower-alpha" /><ref name="S. Poliak & E. Peles" group="lower-alpha" /><ref name=":2" group="lower-alpha" /> 。髓鞘形成主要存在于脊椎动物中，但是在一些无脊椎动物中也发现了类似的系统，比如某些种类的虾<ref name=":3" group="lower-alpha" /> 。脊椎动物中并不是所有的神经元都是有髓神经元; 例如，组成自主神经系统的神经元的轴突一般都不是有髓神经元。

Myelin prevents ions from entering or leaving the axon along myelinated segments. As a general rule, myelination increases the [[conduction velocity]] of action potentials and makes them more energy-efficient. Whether saltatory or not, the mean conduction velocity of an action potential ranges from 1&nbsp;[[Metre per second|meter per second]] (m/s) to over 100&nbsp;m/s, and, in general, increases with axonal diameter.<ref name="hursh_1939" group=lower-alpha>{{cite journal | vauthors = Hursh JB | year = 1939 | title = Conduction velocity and diameter of nerve fibers | journal = American Journal of Physiology | volume = 127 | pages = 131–39| doi = 10.1152/ajplegacy.1939.127.1.131 }}</ref>

Myelin prevents ions from entering or leaving the axon along myelinated segments. As a general rule, myelination increases the [[conduction velocity]] of action potentials and makes them more energy-efficient. Whether saltatory or not, the mean conduction velocity of an action potential ranges from 1&nbsp;[[Metre per second|meter per second]] (m/s) to over 100&nbsp;m/s, and, in general, increases with axonal diameter.<ref name="hursh_1939" group=lower-alpha>{{cite journal | vauthors = Hursh JB | year = 1939 | title = Conduction velocity and diameter of nerve fibers | journal = American Journal of Physiology | volume = 127 | pages = 131–39| doi = 10.1152/ajplegacy.1939.127.1.131 }}</ref>

髓鞘阻止离子沿着髓鞘段进入或离开轴突。作为一般规律，髓鞘形成增加了动作电位的传导速度，使其能量效率更高。不管是否跳跃，动作电位的平均传导速度范围从1米每秒(m/s)到100m/s 以上，一般而言，随轴突直径的增大而增大。

髓鞘阻止离子沿着髓鞘段进入或离开轴突。作为一般规律，髓鞘形成增加了动作电位的传导速度，使其能量效率更高。不管是否跳跃，动作电位的平均传导速度范围从1米每秒(m/s)到100m/s 以上，一般而言，随轴突直径的增大而增大。

Action potentials cannot propagate through the membrane in myelinated segments of the axon. However, the current is carried by the cytoplasm, which is sufficient to depolarize the first or second subsequent [[node of Ranvier]]. Instead, the ionic current from an action potential at one [[node of Ranvier]] provokes another action potential at the next node; this apparent "hopping" of the action potential from node to node is known as [[saltatory conduction]]. Although the mechanism of saltatory conduction was suggested in 1925 by Ralph Lillie,<ref group=lower-alpha>{{cite journal | vauthors = Lillie RS | title = Factors Affecting Transmission and Recovery in the Passive Iron Nerve Model | journal = The Journal of General Physiology | volume = 7 | issue = 4 | pages = 473–507 | date = March 1925 | pmid = 19872151 | pmc = 2140733 | doi = 10.1085/jgp.7.4.473 }} See also {{harvnb|Keynes|Aidley|1991|p=78}}</ref> the first experimental evidence for saltatory conduction came from [[Ichiji Tasaki]]<ref name="tasaki_1939" group=lower-alpha>{{cite journal | vauthors = Tasaki I | year = 1939 | title = Electro-saltatory transmission of nerve impulse and effect of narcosis upon nerve fiber | journal = Am. J. Physiol. | volume = 127 | pages = 211–27| doi = 10.1152/ajplegacy.1939.127.2.211 }}</ref> and Taiji Takeuchi<ref name="tasaki_1941_1942_1959" group=lower-alpha>{{cite journal | vauthors = Tasaki I, Takeuchi T | year = 1941 | title = Der am Ranvierschen Knoten entstehende Aktionsstrom und seine Bedeutung für die Erregungsleitung | journal = Pflügers Archiv für die gesamte Physiologie | volume = 244 | pages = 696–711 | doi = 10.1007/BF01755414 | issue = 6 | s2cid = 8628858 }}<br />* {{cite journal | vauthors = Tasaki I, Takeuchi T | year = 1942 | title = Weitere Studien über den Aktionsstrom der markhaltigen Nervenfaser und über die elektrosaltatorische Übertragung des nervenimpulses | journal = Pflügers Archiv für die gesamte Physiologie | volume = 245 | pages = 764–82 | doi = 10.1007/BF01755237 | issue = 5 | s2cid = 44315437 }}</ref><ref>Tasaki, I in {{harvnb|Field|1959|pp=75–121}}</ref> and from [[Andrew Huxley]] and Robert Stämpfli.<ref name="huxley_staempfli_1949_1951" group=lower-alpha>{{cite journal | vauthors = Huxley AF, Stämpfli R | title = Evidence for saltatory conduction in peripheral myelinated nerve fibres | journal = The Journal of Physiology | volume = 108 | issue = 3 | pages = 315–39 | date = May 1949 | pmid = 16991863 | pmc = 1392492 | doi = 10.1113/jphysiol.1949.sp004335 | author-link1 = Andrew Huxley }}<br />* {{cite journal | vauthors = Huxley AF, Stampfli R | title = Direct determination of membrane resting potential and action potential in single myelinated nerve fibers | journal = The Journal of Physiology | volume = 112 | issue = 3–4 | pages = 476–95 | date = February 1951 | pmid = 14825228 | pmc = 1393015 | doi = 10.1113/jphysiol.1951.sp004545 | author-link1 = Andrew Huxley }}</ref> By contrast, in unmyelinated axons, the action potential provokes another in the membrane immediately adjacent, and moves continuously down the axon like a wave.

Action potentials cannot propagate through the membrane in myelinated segments of the axon. However, the current is carried by the cytoplasm, which is sufficient to depolarize the first or second subsequent [[node of Ranvier]]. Instead, the ionic current from an action potential at one [[node of Ranvier]] provokes another action potential at the next node; this apparent "hopping" of the action potential from node to node is known as [[saltatory conduction]]. Although the mechanism of saltatory conduction was suggested in 1925 by Ralph Lillie,<ref group="lower-alpha" name=":4">{{cite journal | vauthors = Lillie RS | title = Factors Affecting Transmission and Recovery in the Passive Iron Nerve Model | journal = The Journal of General Physiology | volume = 7 | issue = 4 | pages = 473–507 | date = March 1925 | pmid = 19872151 | pmc = 2140733 | doi = 10.1085/jgp.7.4.473 }} See also {{harvnb|Keynes|Aidley|1991|p=78}}</ref> the first experimental evidence for saltatory conduction came from [[Ichiji Tasaki]]<ref name="tasaki_1939" group=lower-alpha>{{cite journal | vauthors = Tasaki I | year = 1939 | title = Electro-saltatory transmission of nerve impulse and effect of narcosis upon nerve fiber | journal = Am. J. Physiol. | volume = 127 | pages = 211–27| doi = 10.1152/ajplegacy.1939.127.2.211 }}</ref> and Taiji Takeuchi<ref name="tasaki_1941_1942_1959" group=lower-alpha>{{cite journal | vauthors = Tasaki I, Takeuchi T | year = 1941 | title = Der am Ranvierschen Knoten entstehende Aktionsstrom und seine Bedeutung für die Erregungsleitung | journal = Pflügers Archiv für die gesamte Physiologie | volume = 244 | pages = 696–711 | doi = 10.1007/BF01755414 | issue = 6 | s2cid = 8628858 }}<br />* {{cite journal | vauthors = Tasaki I, Takeuchi T | year = 1942 | title = Weitere Studien über den Aktionsstrom der markhaltigen Nervenfaser und über die elektrosaltatorische Übertragung des nervenimpulses | journal = Pflügers Archiv für die gesamte Physiologie | volume = 245 | pages = 764–82 | doi = 10.1007/BF01755237 | issue = 5 | s2cid = 44315437 }}</ref><ref name=":12">Tasaki, I in {{harvnb|Field|1959|pp=75–121}}</ref> and from [[Andrew Huxley]] and Robert Stämpfli.<ref name="huxley_staempfli_1949_1951" group=lower-alpha>{{cite journal | vauthors = Huxley AF, Stämpfli R | title = Evidence for saltatory conduction in peripheral myelinated nerve fibres | journal = The Journal of Physiology | volume = 108 | issue = 3 | pages = 315–39 | date = May 1949 | pmid = 16991863 | pmc = 1392492 | doi = 10.1113/jphysiol.1949.sp004335 | author-link1 = Andrew Huxley }}<br />* {{cite journal | vauthors = Huxley AF, Stampfli R | title = Direct determination of membrane resting potential and action potential in single myelinated nerve fibers | journal = The Journal of Physiology | volume = 112 | issue = 3–4 | pages = 476–95 | date = February 1951 | pmid = 14825228 | pmc = 1393015 | doi = 10.1113/jphysiol.1951.sp004545 | author-link1 = Andrew Huxley }}</ref> By contrast, in unmyelinated axons, the action potential provokes another in the membrane immediately adjacent, and moves continuously down the axon like a wave.

动作电位不能在轴突有髓段的膜上传播。然而，电流是由细胞质携带的，这足以使兰花的第一个或第二个后续节点去极化。相反，Ranvier 的一个节点上的动作电位产生的离子电流在下一个节点上激发了另一个动作电位; 这种从一个节点到另一个节点的明显的动作电位“跳跃”被称为跳跃式传导。虽然跳跃式传导的机制在1925年由 Ralph Lillie 提出，但是参见第一个关于跳跃式传导的实验证据来自 Ichiji Tasaki 和 Taiji Takeuchi < br/> Tasaki，i in 和来自 Andrew Huxley 和 Robert Stämpfli。相比之下，在无髓鞘的轴突中，动作电位在紧邻的膜上激发了另一个动作电位，并像波一样不断地沿着轴突移动。

动作电位不能在轴突有髓段的膜上传播。然而，电流是由细胞质携带的，这足以使兰花的第一个或第二个后续节点去极化。相反，Ranvier 的一个节点上的动作电位产生的离子电流在下一个节点上激发了另一个动作电位; 这种从一个节点到另一个节点的明显的动作电位“跳跃”被称为跳跃式传导。虽然跳跃式传导的机制在1925年由 Ralph Lillie 提出,<ref name=":4" group="lower-alpha" /> t，但是参见第一个关于跳跃式传导的实验证据来自 Ichiji Tasaki 和 Taiji Takeuchi <ref name="tasaki_1939" group="lower-alpha" />< br/> Tasaki，i<ref name="tasaki_1941_1942_1959" group="lower-alpha" /><ref name=":12" /> ani in 和来自 Andrew Huxley 和 Robert Stämpflii.<ref name="huxley_staempfli_1949_1951" group="lower-alpha" /> B。相比之下，在无髓鞘的轴突中，动作电位在紧邻的膜上激发了另一个动作电位，并像波一样不断地沿着轴突移动。

[[Image:Conduction velocity and myelination.png|thumb|right|300px|Comparison of the [[conduction velocity|conduction velocities]] of myelinated and unmyelinated [[axon]]s in the [[cat]].{{sfn|Schmidt-Nielsen|1997|loc=Figure 12.13}} The conduction velocity ''v'' of myelinated neurons varies roughly linearly with axon diameter ''d'' (that is, ''v'' ∝ ''d''),<ref name="hursh_1939" group=lower-alpha /> whereas the speed of unmyelinated neurons varies roughly as the square root (''v'' ∝{{radic|''d''}}).<ref name="rushton_1951" group=lower-alpha>{{cite journal | vauthors = Rushton WA | title = A theory of the effects of fibre size in medullated nerve | journal = The Journal of Physiology | volume = 115 | issue = 1 | pages = 101–22 | date = September 1951 | pmid = 14889433 | pmc = 1392008 | doi = 10.1113/jphysiol.1951.sp004655 | author-link = W. A. H. Rushton }}</ref> The red and blue curves are fits of experimental data, whereas the dotted lines are their theoretical extrapolations.|链接=Special:FilePath/Conduction_velocity_and_myelination.png]]

[[Image:Conduction velocity and myelination.png|thumb|right|300px|Comparison of the [[conduction velocity|conduction velocities]] of myelinated and unmyelinated [[axon]]s in the [[cat]].{{sfn|Schmidt-Nielsen|1997|loc=Figure 12.13}} The conduction velocity ''v'' of myelinated neurons varies roughly linearly with axon diameter ''d'' (that is, ''v'' ∝ ''d''),<ref name="hursh_1939" group=lower-alpha /> whereas the speed of unmyelinated neurons varies roughly as the square root (''v'' ∝{{radic|''d''}}).<ref name="rushton_1951" group=lower-alpha>{{cite journal | vauthors = Rushton WA | title = A theory of the effects of fibre size in medullated nerve | journal = The Journal of Physiology | volume = 115 | issue = 1 | pages = 101–22 | date = September 1951 | pmid = 14889433 | pmc = 1392008 | doi = 10.1113/jphysiol.1951.sp004655 | author-link = W. A. H. Rushton }}</ref> The red and blue curves are fits of experimental data, whereas the dotted lines are their theoretical extrapolations.|链接=Special:FilePath/Conduction_velocity_and_myelination.png]]

Myelin has two important advantages: fast conduction speed and energy efficiency. For axons larger than a minimum diameter (roughly 1 [[micrometre]]), myelination increases the [[conduction velocity]] of an action potential, typically tenfold.<ref name="hartline_2007" group=lower-alpha /> Conversely, for a given conduction velocity, myelinated fibers are smaller than their unmyelinated counterparts. For example, action potentials move at roughly the same speed (25&nbsp;m/s) in a myelinated frog axon and an unmyelinated [[squid giant axon]], but the frog axon has a roughly 30-fold smaller diameter and 1000-fold smaller cross-sectional area. Also, since the ionic currents are confined to the nodes of Ranvier, far fewer ions "leak" across the membrane, saving metabolic energy. This saving is a significant [[natural selection|selective advantage]], since the human nervous system uses approximately 20% of the body's metabolic energy.<ref name="hartline_2007" group=lower-alpha>{{cite journal | vauthors = Hartline DK, Colman DR | title = Rapid conduction and the evolution of giant axons and myelinated fibers | journal = Current Biology | volume = 17 | issue = 1 | pages = R29-35 | date = January 2007 | pmid = 17208176 | doi = 10.1016/j.cub.2006.11.042 | s2cid = 10033356 | doi-access = free }}</ref>

Myelin has two important advantages: fast conduction speed and energy efficiency. For axons larger than a minimum diameter (roughly 1 [[micrometre]]), myelination increases the [[conduction velocity]] of an action potential, typically tenfold.<ref name="hartline_2007" group=lower-alpha /> Conversely, for a given conduction velocity, myelinated fibers are smaller than their unmyelinated counterparts. For example, action potentials move at roughly the same speed (25&nbsp;m/s) in a myelinated frog axon and an unmyelinated [[squid giant axon]], but the frog axon has a roughly 30-fold smaller diameter and 1000-fold smaller cross-sectional area. Also, since the ionic currents are confined to the nodes of Ranvier, far fewer ions "leak" across the membrane, saving metabolic energy. This saving is a significant [[natural selection|selective advantage]], since the human nervous system uses approximately 20% of the body's metabolic energy.<ref name="hartline_2007" group=lower-alpha>{{cite journal | vauthors = Hartline DK, Colman DR | title = Rapid conduction and the evolution of giant axons and myelinated fibers | journal = Current Biology | volume = 17 | issue = 1 | pages = R29-35 | date = January 2007 | pmid = 17208176 | doi = 10.1016/j.cub.2006.11.042 | s2cid = 10033356 | doi-access = free }}</ref>

髓鞘具有两个重要的优点: 传导速度快和能量效率高。对于大于最小直径(大约1微米)的轴突，髓鞘形成增加了动作电位的传导速度，通常是原来的十倍。相反，对于一定的传导速度，有髓纤维比无髓纤维小。例如，在有髓青蛙轴突和无髓青蛙轴突中，动作电位的移动速度大致相同(25米/秒) ，但是青蛙轴突的直径要小30倍，横截面积要小1000倍。此外，由于离子电流仅限于郎飞结，跨膜“泄漏”的离子要少得多，从而节省了新陈代谢能量。这种节省是一个重大的选择优势，因为人类神经系统消耗大约20% 的身体代谢能量。

髓鞘具有两个重要的优点: 传导速度快和能量效率高。对于大于最小直径(大约1微米)的轴突，髓鞘形成增加了动作电位的传导速度，通常是原来的十倍.<ref name="hartline_2007" group="lower-alpha" /> Co。相反，对于一定的传导速度，有髓纤维比无髓纤维小。例如，在有髓青蛙轴突和无髓青蛙轴突中，动作电位的移动速度大致相同(25米/秒) ，但是青蛙轴突的直径要小30倍，横截面积要小1000倍。此外，由于离子电流仅限于郎飞结，跨膜“泄漏”的离子要少得多，从而节省了新陈代谢能量。这种节省是一个重大的选择优势，因为人类神经系统消耗大约20% 的身体代谢能量.<ref name="hartline_2007" group="lower-alpha" />。

The length of axons' myelinated segments is important to the success of saltatory conduction. They should be as long as possible to maximize the speed of conduction, but not so long that the arriving signal is too weak to provoke an action potential at the next node of Ranvier. In nature, myelinated segments are generally long enough for the passively propagated signal to travel for at least two nodes while retaining enough amplitude to fire an action potential at the second or third node. Thus, the [[safety factor]] of saltatory conduction is high, allowing transmission to bypass nodes in case of injury. However, action potentials may end prematurely in certain places where the safety factor is low, even in unmyelinated neurons; a common example is the branch point of an axon, where it divides into two axons.{{sfn|Bullock|Orkand|Grinnell|1977|p=163}}

The length of axons' myelinated segments is important to the success of saltatory conduction. They should be as long as possible to maximize the speed of conduction, but not so long that the arriving signal is too weak to provoke an action potential at the next node of Ranvier. In nature, myelinated segments are generally long enough for the passively propagated signal to travel for at least two nodes while retaining enough amplitude to fire an action potential at the second or third node. Thus, the [[safety factor]] of saltatory conduction is high, allowing transmission to bypass nodes in case of injury. However, action potentials may end prematurely in certain places where the safety factor is low, even in unmyelinated neurons; a common example is the branch point of an axon, where it divides into two axons.{{sfn|Bullock|Orkand|Grinnell|1977|p=163}}

轴突有髓神经节段的长度对跳跃式传导的成功至关重要。它们应该尽可能长，以最大限度地提高传导速度，但不能太长，以至于到达的信号太弱，无法在兰维叶的下一个节点激发动作电位。在自然界中，有髓节段通常足够长，使传播的被动信号传播至少两个节点，同时保持足够的振幅，在第二或第三节点激发动作电位。因此，跳跃式传导的安全系数很高，在受伤的情况下可以通过旁路传播。然而，动作电位可能在安全系数较低的某些地方过早终止，甚至在无髓神经元中也是如此; 一个常见的例子是轴突的分支点，在那里它分裂成两个轴突。

轴突有髓神经节段的长度对跳跃式传导的成功至关重要。它们应该尽可能长，以最大限度地提高传导速度，但不能太长，以至于到达的信号太弱，无法在兰维叶的下一个节点激发动作电位。在自然界中，有髓节段通常足够长，使传播的被动信号传播至少两个节点，同时保持足够的振幅，在第二或第三节点激发动作电位。因此，跳跃式传导的安全系数很高，在受伤的情况下可以通过旁路传播。然而，动作电位可能在安全系数较低的某些地方过早终止，甚至在无髓神经元中也是如此; 一个常见的例子是轴突的分支点，在那里它分裂成两个轴突。

Some diseases degrade myelin and impair saltatory conduction, reducing the conduction velocity of action potentials.<ref group=lower-alpha>{{cite journal | vauthors = Miller RH, Mi S | title = Dissecting demyelination | journal = Nature Neuroscience | volume = 10 | issue = 11 | pages = 1351–4 | date = November 2007 | pmid = 17965654 | doi = 10.1038/nn1995 | s2cid = 12441377 }}</ref> The most well-known of these is [[multiple sclerosis]], in which the breakdown of myelin impairs coordinated movement.<ref>Waxman, SG in {{harvnb|Waxman|2007|loc=''Multiple Sclerosis as a Neurodegenerative Disease'', pp. 333–346.}}</ref>

Some diseases degrade myelin and impair saltatory conduction, reducing the conduction velocity of action potentials.<ref group="lower-alpha" name=":5">{{cite journal | vauthors = Miller RH, Mi S | title = Dissecting demyelination | journal = Nature Neuroscience | volume = 10 | issue = 11 | pages = 1351–4 | date = November 2007 | pmid = 17965654 | doi = 10.1038/nn1995 | s2cid = 12441377 }}</ref> The most well-known of these is [[multiple sclerosis]], in which the breakdown of myelin impairs coordinated movement.<ref name=":13">Waxman, SG in {{harvnb|Waxman|2007|loc=''Multiple Sclerosis as a Neurodegenerative Disease'', pp. 333–346.}}</ref>

Waxman, SG in  

Waxman, SG in  

===Cable theory===

===Cable theory===

[[File:Cable theory Neuron RC circuit v3.svg|thumb|300x300px|Cable theory's simplified view of a neuronal fiber. The connected [[RC circuit]]s correspond to adjacent segments of a passive [[neurite]]. The extracellular resistances ''r_e'' (the counterparts of the intracellular resistances ''r_i'') are not shown, since they are usually negligibly small; the extracellular medium may be assumed to have the same voltage everywhere.|链接=Special:FilePath/Cable_theory_Neuron_RC_circuit_v3.svg]]

[[File:Cable theory Neuron RC circuit v3.svg|thumb|300x300px|Cable theory's simplified view of a neuronal fiber. The connected [[RC circuit]]s correspond to adjacent segments of a passive [[neurite]]. The extracellular resistances ''r_e'' (the counterparts of the intracellular resistances ''r_i'') are not shown, since they are usually negligibly small; the extracellular medium may be assumed to have the same voltage everywhere.|链接=Special:FilePath/Cable_theory_Neuron_RC_circuit_v3.svg]]

The flow of currents within an axon can be described quantitatively by [[cable theory]]<ref name="rall_1989">[[Wilfrid Rall|Rall, W]] in {{harvnb|Koch|Segev|1989|loc=''Cable Theory for Dendritic Neurons'', pp. 9–62.}}</ref> and its elaborations, such as the compartmental model.<ref name="segev_1989">{{cite book | vauthors = Segev I, Fleshman JW, Burke RE | chapter = Compartmental Models of Complex Neurons | title = Methods in Neuronal Modeling: From Synapses to Networks. | veditors = Koch C, Segev I  | editor1-link = Christof Koch | date = 1989 | pages = 63–96 | publisher = The MIT Press | location = Cambridge, Massachusetts | isbn = 978-0-262-11133-1 | lccn = 88008279 | oclc = 18384545 }}</ref> Cable theory was developed in 1855 by [[William Thomson, 1st Baron Kelvin|Lord Kelvin]] to model the transatlantic telegraph cable<ref name="kelvin_1855" group=lower-alpha>{{cite journal | vauthors = Kelvin WT | year = 1855 | title = On the theory of the electric telegraph | journal = Proceedings of the Royal Society | volume = 7 | pages = 382–99 | doi = 10.1098/rspl.1854.0093| s2cid = 178547827 | author-link = William Thomson, 1st Baron Kelvin }}</ref> and was shown to be relevant to neurons by [[Alan Lloyd Hodgkin|Hodgkin]] and [[W. A. H. Rushton|Rushton]] in 1946.<ref name="hodgkin_1946" group=lower-alpha>{{cite journal | vauthors = Hodgkin AL, Rushton WA | title = The electrical constants of a crustacean nerve fibre | journal = Proceedings of the Royal Society of Medicine | volume = 134 | issue = 873 | pages = 444–79 | date = December 1946 | pmid = 20281590 | doi = 10.1098/rspb.1946.0024 | author-link1 = Alan Lloyd Hodgkin | bibcode = 1946RSPSB.133..444H | doi-access = free }}</ref> In simple cable theory, the neuron is treated as an electrically passive, perfectly cylindrical transmission cable, which can be described by a [[partial differential equation]]<ref name="rall_1989" />

The flow of currents within an axon can be described quantitatively by [[cable theory]]<ref name="rall_1989">[[Wilfrid Rall|Rall, W]] in {{harvnb|Koch|Segev|1989|loc=''Cable Theory for Dendritic Neurons'', pp. 9–62.}}</ref> and its elaborations, such as the compartmental model.<ref name="segev_1989">{{cite book | vauthors = Segev I, Fleshman JW, Burke RE | chapter = Compartmental Models of Complex Neurons | title = Methods in Neuronal Modeling: From Synapses to Networks. | veditors = Koch C, Segev I  | editor1-link = Christof Koch | date = 1989 | pages = 63–96 | publisher = The MIT Press | location = Cambridge, Massachusetts | isbn = 978-0-262-11133-1 | lccn = 88008279 | oclc = 18384545 }}</ref> Cable theory was developed in 1855 by [[William Thomson, 1st Baron Kelvin|Lord Kelvin]] to model the transatlantic telegraph cable<ref name="kelvin_1855" group=lower-alpha>{{cite journal | vauthors = Kelvin WT | year = 1855 | title = On the theory of the electric telegraph | journal = Proceedings of the Royal Society | volume = 7 | pages = 382–99 | doi = 10.1098/rspl.1854.0093| s2cid = 178547827 | author-link = William Thomson, 1st Baron Kelvin }}</ref> and was shown to be relevant to neurons by [[Alan Lloyd Hodgkin|Hodgkin]] and [[W. A. H. Rushton|Rushton]] in 1946.<ref name="hodgkin_1946" group=lower-alpha>{{cite journal | vauthors = Hodgkin AL, Rushton WA | title = The electrical constants of a crustacean nerve fibre | journal = Proceedings of the Royal Society of Medicine | volume = 134 | issue = 873 | pages = 444–79 | date = December 1946 | pmid = 20281590 | doi = 10.1098/rspb.1946.0024 | author-link1 = Alan Lloyd Hodgkin | bibcode = 1946RSPSB.133..444H | doi-access = free }}</ref> In simple cable theory, the neuron is treated as an electrically passive, perfectly cylindrical transmission cable, which can be described by a [[partial differential equation]]<ref name="rall_1989" />

= = = = 电缆理论 = = = 轴突内电流的流动可以用电缆理论来定量描述。凯布尔理论是在1855年由开尔文勋爵发展起来用来模拟跨大西洋电报电缆的，并在1946年被 Hodgkin 和 Rushton 证明与神经元有关。在简单的电缆理论中，神经元被看作是一根完美的电无源圆柱形传输电缆，可以用偏微分方程来描述

= = = = 电缆理论 = = = 轴突内电流的流动可以用电缆理论来定量描述<ref name="rall_1989" /> 。.<ref name="segev_1989" /> 凯布尔理论是在1855年由开尔文勋爵发展起来用来模拟跨大西洋电报电缆的ble<ref name="kelvin_1855" group="lower-alpha" /> a，并在1946年被 Hodgkin 和 Rushton 证明与神经元有关6.<ref name="hodgkin_1946" group="lower-alpha" /> 。在简单的电缆理论中，神经元被看作是一根完美的电无源圆柱形传输电缆，可以用偏微分方程来描述<ref name="rall_1989" />

:<math>

:<math>

\tau \frac{\partial V}{\partial t} = \lambda^2 \frac{\partial^2 V}{\partial x^2} - V

\tau \frac{\partial V}{\partial t} = \lambda^2 \frac{\partial^2 V}{\partial x^2} - V

</math>

</math>

\tau \frac{\partial V}{\partial t} = \lambda^2 \frac{\partial^2 V}{\partial x^2} - V

\tau \frac{\partial V}{\partial t} = \lambda^2 \frac{\partial^2 V}{\partial x^2} - V

\tau =\ r_m c_m \,

\tau =\ r_m c_m \,

</math>

</math>

\tau =\ r_m c_m \,

\tau =\ r_m c_m \,

\lambda = \sqrt \frac{r_m}{r_\ell}

\lambda = \sqrt \frac{r_m}{r_\ell}

</math>

</math>

\lambda = \sqrt \frac{r_m}{r_\ell}

\lambda = \sqrt \frac{r_m}{r_\ell}

These time and length-scales can be used to understand the dependence of the conduction velocity on the diameter of the neuron in unmyelinated fibers. For example, the time-scale τ increases with both the membrane resistance ''r_m'' and capacitance ''c_m''. As the capacitance increases, more charge must be transferred to produce a given transmembrane voltage (by [[capacitance|the equation ''Q''&nbsp;=&nbsp;''CV'']]); as the resistance increases, less charge is transferred per unit time, making the equilibration slower. In a similar manner, if the internal resistance per unit length ''r_i'' is lower in one axon than in another (e.g., because the radius of the former is larger), the spatial decay length λ becomes longer and the [[conduction velocity]] of an action potential should increase. If the transmembrane resistance ''r_m'' is increased, that lowers the average "leakage" current across the membrane, likewise causing ''λ'' to become longer, increasing the conduction velocity.

These time and length-scales can be used to understand the dependence of the conduction velocity on the diameter of the neuron in unmyelinated fibers. For example, the time-scale τ increases with both the membrane resistance ''r_m'' and capacitance ''c_m''. As the capacitance increases, more charge must be transferred to produce a given transmembrane voltage (by [[capacitance|the equation ''Q''&nbsp;=&nbsp;''CV'']]); as the resistance increases, less charge is transferred per unit time, making the equilibration slower. In a similar manner, if the internal resistance per unit length ''r_i'' is lower in one axon than in another (e.g., because the radius of the former is larger), the spatial decay length λ becomes longer and the [[conduction velocity]] of an action potential should increase. If the transmembrane resistance ''r_m'' is increased, that lowers the average "leakage" current across the membrane, likewise causing ''λ'' to become longer, increasing the conduction velocity.

这些时间尺度和长度尺度可以用来理解传导速度与无髓纤维神经元直径的关系。例如，时间尺度 τ 随着膜电阻 rm 和膜电容 cm 的增大而增大。随着电容的增加，必须转移更多的电荷才能产生给定的跨膜电压(用 q = CV 方程式) ; 随着电阻的增加，每单位时间转移的电荷越少，平衡速度越慢。同样，如果一个轴突的单位长度 ri 内阻低于另一个轴突(例如，因为前者的半径较大) ，空间衰减长度 λ 变长，动作电位的传导速度应该增加。如果跨膜电阻 rm 增大，则降低了跨膜平均“泄漏”电流，同样导致 λ 变长，增加了传导速度。

这些时间尺度和长度尺度可以用来理解传导速度与无髓纤维神经元直径的关系。例如，时间尺度 τ 随着膜电阻 rm 和膜电容 cm 的增大而增大。随着电容的增加，必须转移更多的电荷才能产生给定的跨膜电压(用 q = CV 方程式) ; 随着电阻的增加，每单位时间转移的电荷越少，平衡速度越慢。同样，如果一个轴突的单位长度 ri 内阻低于另一个轴突(例如，因为前者的半径较大) ，空间衰减长度 λ 变长，动作电位的传导速度应该增加。如果跨膜电阻 rm 增大，则降低了跨膜平均“泄漏”电流，同样导致 λ 变长，增加了传导速度。

==Termination==

==Termination 终止==

 

===Chemical synapses化学突触===

In general, action potentials that reach the synaptic knobs cause a [[neurotransmitter]] to be released into the synaptic cleft.<ref group="lower-alpha" name=":6">{{cite book | vauthors = Süudhof TC | title = Pharmacology of Neurotransmitter Release | chapter = Neurotransmitter release | volume = 184 | issue = 184 | pages = 1–21 | year = 2008 | pmid = 18064409 | doi = 10.1007/978-3-540-74805-2_1 | isbn = 978-3-540-74804-5 | series = Handbook of Experimental Pharmacology }}</ref> Neurotransmitters are small molecules that may open ion channels in the postsynaptic cell; most axons have the same neurotransmitter at all of their termini. The arrival of the action potential opens voltage-sensitive calcium channels in the presynaptic membrane; the influx of calcium causes [[synaptic vesicle|vesicles]] filled with neurotransmitter to migrate to the cell's surface and [[exocytosis|release their contents]] into the [[synaptic cleft]].<ref group="lower-alpha" name=":7">{{cite journal | vauthors = Rusakov DA | title = Ca2+-dependent mechanisms of presynaptic control at central synapses | journal = The Neuroscientist | volume = 12 | issue = 4 | pages = 317–26 | date = August 2006 | pmid = 16840708 | pmc = 2684670 | doi = 10.1177/1073858405284672 }}</ref> This complex process is inhibited by the [[neurotoxin]]s [[tetanospasmin]] and [[botulinum toxin]], which are responsible for [[tetanus]] and [[botulism]], respectively.<ref group="lower-alpha" name=":8">{{cite journal | vauthors = Humeau Y, Doussau F, Grant NJ, Poulain B | title = How botulinum and tetanus neurotoxins block neurotransmitter release | journal = Biochimie | volume = 82 | issue = 5 | pages = 427–46 | date = May 2000 | pmid = 10865130 | doi = 10.1016/S0300-9084(00)00216-9 }}</ref>

 

 

===Chemical synapses===

 

In general, action potentials that reach the synaptic knobs cause a [[neurotransmitter]] to be released into the synaptic cleft.<ref group="lower-alpha">{{cite book | vauthors = Süudhof TC | title = Pharmacology of Neurotransmitter Release | chapter = Neurotransmitter release | volume = 184 | issue = 184 | pages = 1–21 | year = 2008 | pmid = 18064409 | doi = 10.1007/978-3-540-74805-2_1 | isbn = 978-3-540-74804-5 | series = Handbook of Experimental Pharmacology }}</ref> Neurotransmitters are small molecules that may open ion channels in the postsynaptic cell; most axons have the same neurotransmitter at all of their termini. The arrival of the action potential opens voltage-sensitive calcium channels in the presynaptic membrane; the influx of calcium causes [[synaptic vesicle|vesicles]] filled with neurotransmitter to migrate to the cell's surface and [[exocytosis|release their contents]] into the [[synaptic cleft]].<ref group=lower-alpha>{{cite journal | vauthors = Rusakov DA | title = Ca2+-dependent mechanisms of presynaptic control at central synapses | journal = The Neuroscientist | volume = 12 | issue = 4 | pages = 317–26 | date = August 2006 | pmid = 16840708 | pmc = 2684670 | doi = 10.1177/1073858405284672 }}</ref> This complex process is inhibited by the [[neurotoxin]]s [[tetanospasmin]] and [[botulinum toxin]], which are responsible for [[tetanus]] and [[botulism]], respectively.<ref group=lower-alpha>{{cite journal | vauthors = Humeau Y, Doussau F, Grant NJ, Poulain B | title = How botulinum and tetanus neurotoxins block neurotransmitter release | journal = Biochimie | volume = 82 | issue = 5 | pages = 427–46 | date = May 2000 | pmid = 10865130 | doi = 10.1016/S0300-9084(00)00216-9 }}</ref>

一般来说，到达突触节点的动作电位会使神经递质释放到突触间隙。神经递质是可以打开突触后细胞离子通道的小分子; 大多数轴突在所有末端都有相同的神经递质。动作电位的到来打开了突触前膜上的电压敏感性钙通道，钙的内流导致充满神经递质的小泡迁移到细胞表面，并将其内容物释放到突触间隙。破伤风和肉毒杆菌毒素分别引起神经毒素破伤风和肉毒杆菌毒素抑制这一复杂的过程。

一般来说，到达突触节点的动作电位会使神经递质释放到突触间隙.<ref name=":6" group="lower-alpha" /> 。神经递质是可以打开突触后细胞离子通道的小分子; 大多数轴突在所有末端都有相同的神经递质。动作电位的到来打开了突触前膜上的电压敏感性钙通道，钙的内流导致充满神经递质的小泡迁移到细胞表面，并将其内容物释放到突触间隙.<ref name=":7" group="lower-alpha" /> 。破伤风和肉毒杆菌毒素分别引起神经毒素破伤风和肉毒杆菌毒素抑制这一复杂的过程.<ref name=":8" group="lower-alpha" />。

[[Image:Gap cell junction-en.svg|thumb|right|[[Electrical synapse]]s between excitable cells allow ions to pass directly from one cell to another, and are much faster than [[chemical synapse]]s.|链接=Special:FilePath/Gap_cell_junction-en.svg]]

[[Image:Gap cell junction-en.svg|thumb|right|[[Electrical synapse]]s between excitable cells allow ions to pass directly from one cell to another, and are much faster than [[chemical synapse]]s.|链接=Special:FilePath/Gap_cell_junction-en.svg]]

===Electrical synapses===

===Electrical synapses===

{{Main|Electrical synapse|Gap junction|Connexin}}

Some synapses dispense with the "middleman" of the neurotransmitter, and connect the presynaptic and postsynaptic cells together.<ref group="lower-alpha" name=":9">{{cite journal | vauthors = Zoidl G, Dermietzel R | title = On the search for the electrical synapse: a glimpse at the future | journal = Cell and Tissue Research | volume = 310 | issue = 2 | pages = 137–42 | date = November 2002 | pmid = 12397368 | doi = 10.1007/s00441-002-0632-x | s2cid = 22414506 }}</ref> When an action potential reaches such a synapse, the ionic currents flowing into the presynaptic cell can cross the barrier of the two cell membranes and enter the postsynaptic cell through pores known as [[connexon]]s.<ref group="lower-alpha" name=":10">{{cite journal | vauthors = Brink PR, Cronin K, Ramanan SV | title = Gap junctions in excitable cells | journal = Journal of Bioenergetics and Biomembranes | volume = 28 | issue = 4 | pages = 351–8 | date = August 1996 | pmid = 8844332 | doi = 10.1007/BF02110111 | s2cid = 46371790 }}</ref> Thus, the ionic currents of the presynaptic action potential can directly stimulate the postsynaptic cell. Electrical synapses allow for faster transmission because they do not require the slow diffusion of [[neurotransmitter]]s across the synaptic cleft. Hence, electrical synapses are used whenever fast response and coordination of timing are crucial, as in [[escape reflex]]es, the [[retina]] of [[vertebrate]]s, and the [[heart]].

Some synapses dispense with the "middleman" of the neurotransmitter, and connect the presynaptic and postsynaptic cells together.<ref group=lower-alpha>{{cite journal | vauthors = Zoidl G, Dermietzel R | title = On the search for the electrical synapse: a glimpse at the future | journal = Cell and Tissue Research | volume = 310 | issue = 2 | pages = 137–42 | date = November 2002 | pmid = 12397368 | doi = 10.1007/s00441-002-0632-x | s2cid = 22414506 }}</ref> When an action potential reaches such a synapse, the ionic currents flowing into the presynaptic cell can cross the barrier of the two cell membranes and enter the postsynaptic cell through pores known as [[connexon]]s.<ref group=lower-alpha>{{cite journal | vauthors = Brink PR, Cronin K, Ramanan SV | title = Gap junctions in excitable cells | journal = Journal of Bioenergetics and Biomembranes | volume = 28 | issue = 4 | pages = 351–8 | date = August 1996 | pmid = 8844332 | doi = 10.1007/BF02110111 | s2cid = 46371790 }}</ref> Thus, the ionic currents of the presynaptic action potential can directly stimulate the postsynaptic cell. Electrical synapses allow for faster transmission because they do not require the slow diffusion of [[neurotransmitter]]s across the synaptic cleft. Hence, electrical synapses are used whenever fast response and coordination of timing are crucial, as in [[escape reflex]]es, the [[retina]] of [[vertebrate]]s, and the [[heart]].

有些突触免除了神经递质的“中间人”，将突触前细胞和突触后细胞连接在一起.<ref name=":9" group="lower-alpha" /> 。当一个动作电位达到这样的突触时，流入突触前细胞的离子电流可以穿过两个细胞膜的屏障，通过称为连接子的孔进入突触后细胞.<ref name=":10" group="lower-alpha" />。因此，突触前动作电位的离子电流可以直接刺激突触后细胞。电突触允许更快的传递，因为它们不需要神经递质在突触间隙中的缓慢扩散。因此，只要快速反应和协调时间是至关重要的，就会使用电突触，例如在逃跑反射、脊椎动物的视网膜和心脏中。

 

===Neuromuscular junctions===

===Neuromuscular junctions===

{{Main|Neuromuscular junction|Acetylcholine receptor|Cholinesterase enzyme}}

A special case of a chemical synapse is the [[neuromuscular junction]], in which the [[axon]] of a [[motor neuron]] terminates on a [[muscle fiber]].<ref group="lower-alpha" name=":11">{{cite journal | vauthors = Hirsch NP | title = Neuromuscular junction in health and disease | journal = British Journal of Anaesthesia | volume = 99 | issue = 1 | pages = 132–8 | date = July 2007 | pmid = 17573397 | doi = 10.1093/bja/aem144 | df = dmy-all | doi-access = free }}</ref> In such cases, the released neurotransmitter is [[acetylcholine]], which binds to the acetylcholine receptor, an integral membrane protein in the membrane (the ''[[sarcolemma]]'') of the muscle fiber.<ref group="lower-alpha" name=":12">{{cite journal | vauthors = Hughes BW, Kusner LL, Kaminski HJ | title = Molecular architecture of the neuromuscular junction | journal = Muscle & Nerve | volume = 33 | issue = 4 | pages = 445–61 | date = April 2006 | pmid = 16228970 | doi = 10.1002/mus.20440 | s2cid = 1888352 }}</ref> However, the acetylcholine does not remain bound; rather, it dissociates and is [[hydrolysis|hydrolyzed]] by the enzyme, [[acetylcholinesterase]], located in the synapse. This enzyme quickly reduces the stimulus to the muscle, which allows the degree and timing of muscular contraction to be regulated delicately. Some poisons inactivate acetylcholinesterase to prevent this control, such as the [[nerve agent]]s [[sarin]] and [[tabun (nerve agent)|tabun]],<ref name=Newmark group=lower-alpha>{{cite journal | vauthors = Newmark J | title = Nerve agents | journal = The Neurologist | volume = 13 | issue = 1 | pages = 20–32 | date = January 2007 | pmid = 17215724 | doi = 10.1097/01.nrl.0000252923.04894.53 | s2cid = 211234081 }}</ref> and the insecticides [[diazinon]] and [[malathion]].<ref group="lower-alpha" name=":13">{{cite journal | vauthors = Costa LG | title = Current issues in organophosphate toxicology | journal = Clinica Chimica Acta; International Journal of Clinical Chemistry | volume = 366 | issue = 1–2 | pages = 1–13 | date = April 2006 | pmid = 16337171 | doi = 10.1016/j.cca.2005.10.008 }}</ref>

A special case of a chemical synapse is the [[neuromuscular junction]], in which the [[axon]] of a [[motor neuron]] terminates on a [[muscle fiber]].<ref group=lower-alpha>{{cite journal | vauthors = Hirsch NP | title = Neuromuscular junction in health and disease | journal = British Journal of Anaesthesia | volume = 99 | issue = 1 | pages = 132–8 | date = July 2007 | pmid = 17573397 | doi = 10.1093/bja/aem144 | df = dmy-all | doi-access = free }}</ref> In such cases, the released neurotransmitter is [[acetylcholine]], which binds to the acetylcholine receptor, an integral membrane protein in the membrane (the ''[[sarcolemma]]'') of the muscle fiber.<ref group=lower-alpha>{{cite journal | vauthors = Hughes BW, Kusner LL, Kaminski HJ | title = Molecular architecture of the neuromuscular junction | journal = Muscle & Nerve | volume = 33 | issue = 4 | pages = 445–61 | date = April 2006 | pmid = 16228970 | doi = 10.1002/mus.20440 | s2cid = 1888352 }}</ref> However, the acetylcholine does not remain bound; rather, it dissociates and is [[hydrolysis|hydrolyzed]] by the enzyme, [[acetylcholinesterase]], located in the synapse. This enzyme quickly reduces the stimulus to the muscle, which allows the degree and timing of muscular contraction to be regulated delicately. Some poisons inactivate acetylcholinesterase to prevent this control, such as the [[nerve agent]]s [[sarin]] and [[tabun (nerve agent)|tabun]],<ref name=Newmark group=lower-alpha>{{cite journal | vauthors = Newmark J | title = Nerve agents | journal = The Neurologist | volume = 13 | issue = 1 | pages = 20–32 | date = January 2007 | pmid = 17215724 | doi = 10.1097/01.nrl.0000252923.04894.53 | s2cid = 211234081 }}</ref> and the insecticides [[diazinon]] and [[malathion]].<ref group=lower-alpha>{{cite journal | vauthors = Costa LG | title = Current issues in organophosphate toxicology | journal = Clinica Chimica Acta; International Journal of Clinical Chemistry | volume = 366 | issue = 1–2 | pages = 1–13 | date = April 2006 | pmid = 16337171 | doi = 10.1016/j.cca.2005.10.008 }}</ref>

突触间隙的一个特例是神经肌肉接点，运动神经元的轴突终止于肌纤维上.<ref name=":11" group="lower-alpha" />。在这种情况下，释放出来的神经递质是乙酰胆碱，它结合在肌肉纤维膜(肌膜)上的乙酰胆碱受体膜内在蛋白.<ref name=":12" group="lower-alpha" />。然而，乙酰胆碱并不保持结合状态，而是分解并被位于突触中的乙酰胆碱酯酶水解。这种酶能迅速减少对肌肉的刺激，从而使肌肉收缩的程度和时间得到精细的调节。一些毒药使乙酰胆碱酯酶失活，以防止这种控制，如神经毒剂沙林和塔崩,<ref name="Newmark" group="lower-alpha" />，以及杀虫剂二嗪农和马拉硫磷.<ref name=":13" group="lower-alpha" />。

 

 

 

 

 

[[Image:Ventricular myocyte action potential.svg|thumb|right|220px|Phases of a cardiac action potential. The sharp rise in voltage ("0") corresponds to the influx of sodium ions, whereas the two decays ("1" and "3", respectively) correspond to the sodium-channel inactivation and the repolarizing eflux of potassium ions. The characteristic plateau ("2") results from the opening of voltage-sensitive [[calcium]] channels.|链接=Special:FilePath/Ventricular_myocyte_action_potential.svg]]

[[Image:Ventricular myocyte action potential.svg|thumb|right|220px|Phases of a cardiac action potential. The sharp rise in voltage ("0") corresponds to the influx of sodium ions, whereas the two decays ("1" and "3", respectively) correspond to the sodium-channel inactivation and the repolarizing eflux of potassium ions. The characteristic plateau ("2") results from the opening of voltage-sensitive [[calcium]] channels.|链接=Special:FilePath/Ventricular_myocyte_action_potential.svg]]

The cardiac action potential differs from the neuronal action potential by having an extended plateau, in which the membrane is held at a high voltage for a few hundred milliseconds prior to being repolarized by the potassium current as usual.<ref name=Kleber group=lower-alpha /> This plateau is due to the action of slower [[calcium]] channels opening and holding the membrane voltage near their equilibrium potential even after the sodium channels have inactivated.

The cardiac action potential differs from the neuronal action potential by having an extended plateau, in which the membrane is held at a high voltage for a few hundred milliseconds prior to being repolarized by the potassium current as usual.<ref name=Kleber group=lower-alpha /> This plateau is due to the action of slower [[calcium]] channels opening and holding the membrane voltage near their equilibrium potential even after the sodium channels have inactivated.

The cardiac action potential plays an important role in coordinating the contraction of the heart.<ref name=Kleber group=lower-alpha>{{cite journal | vauthors = Kléber AG, Rudy Y | title = Basic mechanisms of cardiac impulse propagation and associated arrhythmias | journal = Physiological Reviews | volume = 84 | issue = 2 | pages = 431–88 | date = April 2004 | pmid = 15044680 | doi = 10.1152/physrev.00025.2003 | s2cid = 21823003 }}</ref> The cardiac cells of the [[sinoatrial node]] provide the [[pacemaker potential]] that synchronizes the heart. The action potentials of those cells propagate to and through the [[atrioventricular node]] (AV node), which is normally the only conduction pathway between the [[atrium (heart)|atria]] and the [[ventricle (heart)|ventricles]]. Action potentials from the AV node travel through the [[bundle of His]] and thence to the [[Purkinje fiber]]s.<ref group=note>Note that these [[Purkinje fiber]]s are muscle fibers and not related to the [[Purkinje cell]]s, which are [[neuron]]s found in the [[cerebellum]].</ref> Conversely, anomalies in the cardiac action potential—whether due to a congenital mutation or injury—can lead to human pathologies, especially [[Heart arrhythmia|arrhythmia]]s.<ref name=Kleber group=lower-alpha /> Several anti-arrhythmia drugs act on the cardiac action potential, such as [[quinidine]], [[lidocaine]], [[beta blocker]]s, and [[verapamil]].<ref group=lower-alpha>{{cite journal | vauthors = Tamargo J, Caballero R, Delpón E | title = Pharmacological approaches in the treatment of atrial fibrillation | journal = Current Medicinal Chemistry | volume = 11 | issue = 1 | pages = 13–28 | date = January 2004 | pmid = 14754423 | doi = 10.2174/0929867043456241 }}</ref>

The cardiac action potential plays an important role in coordinating the contraction of the heart.<ref name=Kleber group=lower-alpha>{{cite journal | vauthors = Kléber AG, Rudy Y | title = Basic mechanisms of cardiac impulse propagation and associated arrhythmias | journal = Physiological Reviews | volume = 84 | issue = 2 | pages = 431–88 | date = April 2004 | pmid = 15044680 | doi = 10.1152/physrev.00025.2003 | s2cid = 21823003 }}</ref> The cardiac cells of the [[sinoatrial node]] provide the [[pacemaker potential]] that synchronizes the heart. The action potentials of those cells propagate to and through the [[atrioventricular node]] (AV node), which is normally the only conduction pathway between the [[atrium (heart)|atria]] and the [[ventricle (heart)|ventricles]]. Action potentials from the AV node travel through the [[bundle of His]] and thence to the [[Purkinje fiber]]s.<ref group="note" name=":0">Note that these [[Purkinje fiber]]s are muscle fibers and not related to the [[Purkinje cell]]s, which are [[neuron]]s found in the [[cerebellum]].</ref> Conversely, anomalies in the cardiac action potential—whether due to a congenital mutation or injury—can lead to human pathologies, especially [[Heart arrhythmia|arrhythmia]]s.<ref name=Kleber group=lower-alpha /> Several anti-arrhythmia drugs act on the cardiac action potential, such as [[quinidine]], [[lidocaine]], [[beta blocker]]s, and [[verapamil]].<ref group="lower-alpha" name=":14">{{cite journal | vauthors = Tamargo J, Caballero R, Delpón E | title = Pharmacological approaches in the treatment of atrial fibrillation | journal = Current Medicinal Chemistry | volume = 11 | issue = 1 | pages = 13–28 | date = January 2004 | pmid = 14754423 | doi = 10.2174/0929867043456241 }}</ref>

心脏动作电位在协调心脏收缩中起着重要作用。窦房结的心脏细胞提供了同步心脏的起搏器电位。这些细胞的动作电位传导到并通过房室结，这通常是心房和心室之间唯一的传导通路。房室结的动作电位通过 His 束传递到浦肯野纤维。请注意，这些浦肯野纤维是肌纤维，与浦肯野细胞无关，浦肯野细胞是小脑中的神经元。相反，心脏动作电位的异常ーー无论是由于先天性突变还是损伤ーー都可能导致人类疾病，尤其是心律失常。几种抗心律失常药物作用于心脏动作电位，如奎尼丁、利多卡因、 β 受体阻滞剂和维拉帕米。

心脏动作电位在协调心脏收缩中起着重要作用。窦房结的心脏细胞提供了同步心脏的起搏器电位t.<ref name="Kleber" group="lower-alpha" />。这些细胞的动作电位传导到并通过房室结，这通常是心房和心室之间唯一的传导通路。房室结的动作电位通过 His 束传递到浦肯野纤维。请注意，这些浦肯野纤维是肌纤维，与浦肯野细胞无关，浦肯野细胞是小脑中的神经元.<ref name=":0" group="note" />。相反，心脏动作电位的异常ーー无论是由于先天性突变还是损伤ーー都可能导致人类疾病，尤其是心律失常.<ref name="Kleber" group="lower-alpha" />。几种抗心律失常药物作用于心脏动作电位，如奎尼丁、利多卡因、 β 受体阻滞剂和维拉帕米.<ref name=":14" group="lower-alpha" />。

===Muscular action potentials===

===Muscular action potentials===

The action potential in a normal skeletal muscle cell is similar to the action potential in neurons.{{sfn|Ganong|1991|pp=59–60}} Action potentials result from the depolarization of the cell membrane (the [[sarcolemma]]), which opens voltage-sensitive sodium channels; these become inactivated and the membrane is repolarized through the outward current of potassium ions. The resting potential prior to the action potential is typically −90mV, somewhat more negative than typical neurons. The muscle action potential lasts roughly 2–4&nbsp;ms, the absolute refractory period is roughly 1–3&nbsp;ms, and the conduction velocity along the muscle is roughly 5&nbsp;m/s. The action potential releases [[calcium]] ions that free up the [[tropomyosin]] and allow the muscle to contract. Muscle action potentials are provoked by the arrival of a pre-synaptic neuronal action potential at the [[neuromuscular junction]], which is a common target for [[neurotoxin]]s.<ref name=Newmark group=lower-alpha />

The action potential in a normal skeletal muscle cell is similar to the action potential in neurons.{{sfn|Ganong|1991|pp=59–60}} Action potentials result from the depolarization of the cell membrane (the [[sarcolemma]]), which opens voltage-sensitive sodium channels; these become inactivated and the membrane is repolarized through the outward current of potassium ions. The resting potential prior to the action potential is typically −90mV, somewhat more negative than typical neurons. The muscle action potential lasts roughly 2–4&nbsp;ms, the absolute refractory period is roughly 1–3&nbsp;ms, and the conduction velocity along the muscle is roughly 5&nbsp;m/s. The action potential releases [[calcium]] ions that free up the [[tropomyosin]] and allow the muscle to contract. Muscle action potentials are provoked by the arrival of a pre-synaptic neuronal action potential at the [[neuromuscular junction]], which is a common target for [[neurotoxin]]s.<ref name=Newmark group=lower-alpha />

正常骨骼肌细胞的动作电位与神经元的动作电位相似。动作电位是细胞膜(肌膜)去极化的结果，这种去极化开启了电压敏感的钠通道，这些电压敏感的钠通道失活，膜通过钾离子的外向电流再次极化。动作电位之前的静息电位通常是 -90mV，比典型的神经元稍微负。肌肉动作电位持续时间约为2-4ms，绝对不应期(性)约为1-3ms，肌肉传导速度约为5 m/s。动作电位释放钙离子，释放原肌球蛋白，使肌肉收缩。肌肉动作电位是由突触前神经元动作电位在神经肌肉接点的到达引起的，这是神经毒素的一个共同目标。

正常骨骼肌细胞的动作电位与神经元的动作电位相似。动作电位是细胞膜(肌膜)去极化的结果，这种去极化开启了电压敏感的钠通道，这些电压敏感的钠通道失活，膜通过钾离子的外向电流再次极化。动作电位之前的静息电位通常是 -90mV，比典型的神经元稍微负。肌肉动作电位持续时间约为2-4ms，绝对不应期(性)约为1-3ms，肌肉传导速度约为5 m/s。动作电位释放钙离子，释放原肌球蛋白，使肌肉收缩。肌肉动作电位是由突触前神经元动作电位在神经肌肉接点的到达引起的，这是神经毒素的一个共同目标.<ref name="Newmark" group="lower-alpha" />。

===Plant action potentials===

===Plant action potentials===

[[Plant cells|Plant]] and [[fungi|fungal cells]]<ref name="Slayman_1976" group=lower-alpha>{{cite journal | vauthors = Slayman CL, Long WS, Gradmann D | title = "Action potentials" in Neurospora crassa, a mycelial fungus | journal = Biochimica et Biophysica Acta (BBA) - Biomembranes | volume = 426 | issue = 4 | pages = 732–44 | date = April 1976 | pmid = 130926 | doi = 10.1016/0005-2736(76)90138-3 }}</ref> are also electrically excitable. The fundamental difference from animal action potentials is that the depolarization in plant cells is not accomplished by an uptake of positive sodium ions, but by release of negative ''chloride'' ions.<ref name = "Mummert_1991" group=lower-alpha>{{cite journal | vauthors = Mummert H, Gradmann D | title = Action potentials in Acetabularia: measurement and simulation of voltage-gated fluxes | journal = The Journal of Membrane Biology | volume = 124 | issue = 3 | pages = 265–73 | date = December 1991 | pmid = 1664861 | doi = 10.1007/BF01994359 | s2cid = 22063907 }}</ref><ref name = "Gradmann_2001" group=lower-alpha>{{cite journal | vauthors = Gradmann D | year = 2001 | title = Models for oscillations in plants | journal = Aust. J. Plant Physiol. | volume = 28 | issue = 7 | pages = 577–590 | doi = 10.1071/pp01017}}</ref><ref name="Beilby_2007" group="lower-alpha">{{cite book | vauthors = Beilby MJ | title = Action potential in charophytes | volume = 257 | pages = 43–82 | year = 2007 | pmid = 17280895 | doi = 10.1016/S0074-7696(07)57002-6 | isbn = 978-0-12-373701-4 | series = International Review of Cytology }}</ref>  In 1906, J. C. Bose published the first measurements of action potentials in plants, which had previously been discovered by Burdon-Sanderson and Darwin.<ref name=":14">{{Cite journal|last=Tandon|first=Prakash N|date=2019-07-01|title=Jagdish Chandra Bose and Plant Neurobiology: Part I|url=http://insa.nic.in/writereaddata/UpLoadedFiles/IJHS/Vol54_2_2019__Art05.pdf|journal=Indian Journal of History of Science|volume=54|issue=2|doi=10.16943/ijhs/2019/v54i2/49660|issn=0019-5235|doi-access=free}}</ref>  An increase in cytoplasmic calcium ions may be the cause of anion release into the cell. This makes calcium a precursor to ion movements, such as the influx of negative chloride ions and efflux of positive potassium ions, as seen in barley leaves.<ref name=":15">{{cite journal | vauthors = Felle HH, Zimmermann MR | title = Systemic signalling in barley through action potentials | journal = Planta | volume = 226 | issue = 1 | pages = 203–14 | date = June 2007 | pmid = 17226028 | doi = 10.1007/s00425-006-0458-y | s2cid = 5059716 }}</ref>

 

[[Plant cells|Plant]] and [[fungi|fungal cells]]<ref name="Slayman_1976" group=lower-alpha>{{cite journal | vauthors = Slayman CL, Long WS, Gradmann D | title = "Action potentials" in Neurospora crassa, a mycelial fungus | journal = Biochimica et Biophysica Acta (BBA) - Biomembranes | volume = 426 | issue = 4 | pages = 732–44 | date = April 1976 | pmid = 130926 | doi = 10.1016/0005-2736(76)90138-3 }}</ref> are also electrically excitable. The fundamental difference from animal action potentials is that the depolarization in plant cells is not accomplished by an uptake of positive sodium ions, but by release of negative ''chloride'' ions.<ref name = "Mummert_1991" group=lower-alpha>{{cite journal | vauthors = Mummert H, Gradmann D | title = Action potentials in Acetabularia: measurement and simulation of voltage-gated fluxes | journal = The Journal of Membrane Biology | volume = 124 | issue = 3 | pages = 265–73 | date = December 1991 | pmid = 1664861 | doi = 10.1007/BF01994359 | s2cid = 22063907 }}</ref><ref name = "Gradmann_2001" group=lower-alpha>{{cite journal | vauthors = Gradmann D | year = 2001 | title = Models for oscillations in plants | journal = Aust. J. Plant Physiol. | volume = 28 | issue = 7 | pages = 577–590 | doi = 10.1071/pp01017}}</ref><ref name="Beilby_2007" group="lower-alpha">{{cite book | vauthors = Beilby MJ | title = Action potential in charophytes | volume = 257 | pages = 43–82 | year = 2007 | pmid = 17280895 | doi = 10.1016/S0074-7696(07)57002-6 | isbn = 978-0-12-373701-4 | series = International Review of Cytology }}</ref>  In 1906, J. C. Bose published the first measurements of action potentials in plants, which had previously been discovered by Burdon-Sanderson and Darwin.<ref>{{Cite journal|last=Tandon|first=Prakash N|date=2019-07-01|title=Jagdish Chandra Bose and Plant Neurobiology: Part I|url=http://insa.nic.in/writereaddata/UpLoadedFiles/IJHS/Vol54_2_2019__Art05.pdf|journal=Indian Journal of History of Science|volume=54|issue=2|doi=10.16943/ijhs/2019/v54i2/49660|issn=0019-5235|doi-access=free}}</ref>  An increase in cytoplasmic calcium ions may be the cause of anion release into the cell. This makes calcium a precursor to ion movements, such as the influx of negative chloride ions and efflux of positive potassium ions, as seen in barley leaves.<ref>{{cite journal | vauthors = Felle HH, Zimmermann MR | title = Systemic signalling in barley through action potentials | journal = Planta | volume = 226 | issue = 1 | pages = 203–14 | date = June 2007 | pmid = 17226028 | doi = 10.1007/s00425-006-0458-y | s2cid = 5059716 }}</ref>

植物和真菌细胞也是电性兴奋的。与动物动作电位的根本区别在于，植物细胞的去极化不是通过吸收正钠离子来完成的，而是通过释放负氯离子来完成的。1906年，杰 · c · 博斯发表了植物中第一次动作电位的测量结果，这是之前由伯顿-桑德森和达尔文发现的。细胞质中钙离子的增加可能是阴离子释放到细胞中的原因。这使得钙成为离子运动的前体，例如负氯离子的流入和正钾离子的外流，如在大麦叶片中所见。

植物和真菌细胞<ref name="Slayman_1976" group="lower-alpha" /> 也是电性兴奋的。与动物动作电位的根本区别在于，植物细胞的去极化不是通过吸收正钠离子来完成的，而是通过释放负氯离子来完成的.<ref name="Mummert_1991" group="lower-alpha" /><ref name="Gradmann_2001" group="lower-alpha" />。1906年，杰 · c · 博斯发表了植物中第一次动作电位的测量结果，这是之前由伯顿-桑德森和达尔文发现的.<ref name=":14" />  。细胞质中钙离子的增加可能是阴离子释放到细胞中的原因。这使得钙成为离子运动的前体，例如负氯离子的流入和正钾离子的外流，如在大麦叶片中所见.<ref name=":15" />。

The initial influx of calcium ions also poses a small cellular depolarization, causing the voltage-gated ion channels to open and allowing full depolarization to be propagated by chloride ions.

The initial influx of calcium ions also poses a small cellular depolarization, causing the voltage-gated ion channels to open and allowing full depolarization to be propagated by chloride ions.

钙离子的初始注入也产生了一个小的细胞去极化，导致电压门控离子通道打开并允许氯离子传播完全去极化。

钙离子的初始注入也产生了一个小的细胞去极化，导致电压门控离子通道打开并允许氯离子传播完全去极化。

Some plants (e.g. ''[[Dionaea muscipula]]'') use sodium-gated channels to operate movements and essentially "count". ''Dionaea muscipula'', also known as the Venus flytrap, is found in subtropical wetlands in North and South Carolina.<ref>{{Cite journal|last=Luken|first=James O. | name-list-style = vanc |date= December 2005 |title=Habitats of Dionaea muscipula (Venus' Fly Trap), Droseraceae, Associated with Carolina Bays|journal=Southeastern Naturalist|language=en|volume=4|issue=4|pages=573–584|doi=10.1656/1528-7092(2005)004[0573:HODMVF]2.0.CO;2|issn=1528-7092}}</ref> When there are poor soil nutrients, the flytrap relies on a diet of insects and animals.<ref name=":1">{{cite journal | vauthors = Böhm J, Scherzer S, Krol E, Kreuzer I, von Meyer K, Lorey C, Mueller TD, Shabala L, Monte I, Solano R, Al-Rasheid KA, Rennenberg H, Shabala S, Neher E, Hedrich R | display-authors = 6 | title = The Venus Flytrap Dionaea muscipula Counts Prey-Induced Action Potentials to Induce Sodium Uptake | journal = Current Biology | volume = 26 | issue = 3 | pages = 286–95 | date = February 2016 | pmid = 26804557 | pmc = 4751343 | doi = 10.1016/j.cub.2015.11.057 }}</ref> Despite research on the plant, there lacks an understanding behind the molecular basis to the Venus flytraps, and carnivore plants in general.<ref name=":2">{{cite journal | vauthors = Hedrich R, Neher E | title = Venus Flytrap: How an Excitable, Carnivorous Plant Works | journal = Trends in Plant Science | volume = 23 | issue = 3 | pages = 220–234 | date = March 2018 | pmid = 29336976 | doi = 10.1016/j.tplants.2017.12.004 }}</ref>

Some plants (e.g. ''[[Dionaea muscipula]]'') use sodium-gated channels to operate movements and essentially "count". ''Dionaea muscipula'', also known as the Venus flytrap, is found in subtropical wetlands in North and South Carolina.<ref name=":16">{{Cite journal|last=Luken|first=James O. | name-list-style = vanc |date= December 2005 |title=Habitats of Dionaea muscipula (Venus' Fly Trap), Droseraceae, Associated with Carolina Bays|journal=Southeastern Naturalist|language=en|volume=4|issue=4|pages=573–584|doi=10.1656/1528-7092(2005)004[0573:HODMVF]2.0.CO;2|issn=1528-7092}}</ref> When there are poor soil nutrients, the flytrap relies on a diet of insects and animals.<ref name=":1">{{cite journal | vauthors = Böhm J, Scherzer S, Krol E, Kreuzer I, von Meyer K, Lorey C, Mueller TD, Shabala L, Monte I, Solano R, Al-Rasheid KA, Rennenberg H, Shabala S, Neher E, Hedrich R | display-authors = 6 | title = The Venus Flytrap Dionaea muscipula Counts Prey-Induced Action Potentials to Induce Sodium Uptake | journal = Current Biology | volume = 26 | issue = 3 | pages = 286–95 | date = February 2016 | pmid = 26804557 | pmc = 4751343 | doi = 10.1016/j.cub.2015.11.057 }}</ref> Despite research on the plant, there lacks an understanding behind the molecular basis to the Venus flytraps, and carnivore plants in general.<ref name=":2">{{cite journal | vauthors = Hedrich R, Neher E | title = Venus Flytrap: How an Excitable, Carnivorous Plant Works | journal = Trends in Plant Science | volume = 23 | issue = 3 | pages = 220–234 | date = March 2018 | pmid = 29336976 | doi = 10.1016/j.tplants.2017.12.004 }}</ref>

 

However, plenty of research has been done on action potentials and how they affect movement and clockwork within the Venus flytrap. To start, the resting membrane potential of the Venus flytrap (-120mV) is lower than animal cells (usually -90mV to -40mV).<ref name=":2" /><ref>Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Neuroscience. 2nd edition. Sunderland (MA): Sinauer Associates; 2001. Electrical Potentials Across Nerve Cell Membranes.Available from: <nowiki>https://www.ncbi.nlm.nih.gov/books/NBK11069/</nowiki></ref> The lower resting potential makes it easier to activate an action potential. Thus, when an insect lands on the trap of the plant, it triggers a hair-like mechanoreceptor.<ref name=":2" /> This receptor then activates an action potential which lasts around 1.5 ms.<ref>{{cite journal | vauthors = Volkov AG, Adesina T, Jovanov E | title = Closing of venus flytrap by electrical stimulation of motor cells | journal = Plant Signaling & Behavior | volume = 2 | issue = 3 | pages = 139–45 | date = May 2007 | pmid = 19516982 | pmc = 2634039 | doi = 10.4161/psb.2.3.4217 }}</ref> Ultimately, this causes an increase of positive Calcium ions into the cell, slightly depolarizing it.

一些植物(例如:。捕蝇草)使用钠门控通道操作运动，本质上是“计数”。捕蝇草，也被称为捕蝇草，发现于北卡罗来纳州和南卡罗来纳州的亚热带湿地.<ref name=":16" />。当土壤养分不足时，捕蝇草依靠昆虫和动物为食.<ref name=":1" />。尽管对这种植物进行了研究，但对于金星捕蝇草和一般的食肉植物的分子基础还缺乏了解.<ref name=":2" />。

However, plenty of research has been done on action potentials and how they affect movement and clockwork within the Venus flytrap. To start, the resting membrane potential of the Venus flytrap (-120mV) is lower than animal cells (usually -90mV to -40mV).Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Neuroscience. 2nd edition. Sunderland (MA): Sinauer Associates; 2001. Electrical Potentials Across Nerve Cell Membranes.Available from: https://www.ncbi.nlm.nih.gov/books/NBK11069/ The lower resting potential makes it easier to activate an action potential. Thus, when an insect lands on the trap of the plant, it triggers a hair-like mechanoreceptor. This receptor then activates an action potential which lasts around 1.5 ms. Ultimately, this causes an increase of positive Calcium ions into the cell, slightly depolarizing it.

However, plenty of research has been done on action potentials and how they affect movement and clockwork within the Venus flytrap. To start, the resting membrane potential of the Venus flytrap (-120mV) is lower than animal cells (usually -90mV to -40mV).<ref name=":2" /><ref name=":17">Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Neuroscience. 2nd edition. Sunderland (MA): Sinauer Associates; 2001. Electrical Potentials Across Nerve Cell Membranes.Available from: <nowiki>https://www.ncbi.nlm.nih.gov/books/NBK11069/</nowiki></ref> The lower resting potential makes it easier to activate an action potential. Thus, when an insect lands on the trap of the plant, it triggers a hair-like mechanoreceptor.<ref name=":2" /> This receptor then activates an action potential which lasts around 1.5 ms.<ref name=":18">{{cite journal | vauthors = Volkov AG, Adesina T, Jovanov E | title = Closing of venus flytrap by electrical stimulation of motor cells | journal = Plant Signaling & Behavior | volume = 2 | issue = 3 | pages = 139–45 | date = May 2007 | pmid = 19516982 | pmc = 2634039 | doi = 10.4161/psb.2.3.4217 }}</ref> Ultimately, this causes an increase of positive Calcium ions into the cell, slightly depolarizing it.

然而，已经有很多关于动作电位以及它们如何影响捕蝇草内的运动和钟表的研究。首先，捕蝇草的静息膜电位(- 120mV)低于动物细胞(通常为-90mv 至-40mv)。普夫斯 d，奥古斯丁 GJ，菲茨帕特里克 d，等编辑。神经科学。第二版。桑德兰: Sinauer Associates; 2001。神经细胞膜上的电位。低 https://www.ncbi.nlm.nih.gov/books/nbk11069/的静息电位可以更容易地激活动作电位。因此，当一只昆虫落在植物的陷阱上时，它就会触发一个毛发样的机械感受器。这个受体激活一个持续约1.5毫秒的动作电位。最终，这会导致钙离子进入细胞，使细胞稍微去极化。

然而，已经有很多关于动作电位以及它们如何影响捕蝇草内的运动和钟表的研究。首先，捕蝇草的静息膜电位(- 120mV)低于动物细胞(通常为-90mv 至-40mv).<ref name=":2" /><ref name=":17" />。神经细胞膜上的电位。的静息电位可以更容易地激活动作电位。因此，当一只昆虫落在植物的陷阱上时，它就会触发一个毛发样的机械感受器。.<ref name=":2" /> 低这个受体激活一个持续约1.5毫秒的动作电位.<ref name=":18" /> 。最终，这会导致钙离子进入细胞，使细胞稍微去极化。 [https://www.ncbi.nlm.nih.gov/books/nbk11069/的静息电位可以更容易地激活动作电位。因此，当一只昆虫落在植物的陷阱上时，它就会触发一个毛发样的机械感受器。这个受体激活一个持续约1.5毫秒的动作电位。最终，这会导致钙离子进入细胞，使细胞稍微去极化。 https://www.ncbi.nlm.nih.gov/books/nbk11069/] 

However, the flytrap doesn't close after one trigger. Instead, it requires the activation of 2 or more hairs.<ref name=":1" /><ref name=":2" /> If only one hair is triggered, it throws the activation as a false positive. Further, the second hair must be activated within a certain time interval (0.75 s - 40 s) for it to register with the first activation.<ref name=":2" /> Thus, a buildup of calcium starts and slowly falls from the first trigger. When the second action potential is fired within the time interval, it reaches the Calcium threshold to depolarize the cell, closing the trap on the prey within a fraction of a second.<ref name=":2" />

However, the flytrap doesn't close after one trigger. Instead, it requires the activation of 2 or more hairs.<ref name=":1" /><ref name=":2" /> If only one hair is triggered, it throws the activation as a false positive. Further, the second hair must be activated within a certain time interval (0.75 s - 40 s) for it to register with the first activation.<ref name=":2" /> Thus, a buildup of calcium starts and slowly falls from the first trigger. When the second action potential is fired within the time interval, it reaches the Calcium threshold to depolarize the cell, closing the trap on the prey within a fraction of a second.<ref name=":2" />

然而，捕蝇器不会在一次触发后关闭。相反，它需要激活2根或更多的毛发。如果只有一根头发被触发，它就会将这个激活作为一个假阳性而抛出。此外，第二根头发必须在一定的时间间隔(0.75 s-40 s)内被激活，才能在第一次激活中注册。因此，钙的积累开始并且从第一个触发点开始慢慢下降。当第二个动作电位在时间间隔内被激发时，它达到钙阈值使细胞去极化，在几分之一秒内关闭捕获物的陷阱。

然而，捕蝇器不会在一次触发后关闭。相反，它需要激活2根或更多的毛发.<ref name=":1" /><ref name=":2" /> 。如果只有一根头发被触发，它就会将这个激活作为一个假阳性而抛出。此外，第二根头发必须在一定的时间间隔(0.75 s-40 s)内被激活，才能在第一次激活中注册.<ref name=":2" /> 。因此，钙的积累开始并且从第一个触发点开始慢慢下降。当第二个动作电位在时间间隔内被激发时，它达到钙阈值使细胞去极化，在几分之一秒内关闭捕获物的陷阱.<ref name=":2" /> 。

Together with the subsequent release of positive potassium ions the action potential in plants involves an [[osmotic]] loss of salt (KCl). Whereas, the animal action potential is osmotically neutral because equal amounts of entering sodium and leaving potassium cancel each other osmotically. The interaction of electrical and osmotic relations in plant cells<ref name="Gradmann_1998" group="lower-alpha">{{cite journal | vauthors = Gradmann D, Hoffstadt J | title = Electrocoupling of ion transporters in plants: interaction with internal ion concentrations | journal = The Journal of Membrane Biology | volume = 166 | issue = 1 | pages = 51–9 | date = November 1998 | pmid = 9784585 | doi = 10.1007/s002329900446 | s2cid = 24190001 }}</ref> appears to have arisen from an osmotic function of electrical excitability in a common unicellular ancestors of plants and animals under changing salinity conditions. Further, the present function of rapid signal transmission is seen as a newer accomplishment of [[metazoan]] cells in a more stable osmotic environment.<ref name="Gradmann_1980">

Together with the subsequent release of positive potassium ions the action potential in plants involves an [[osmotic]] loss of salt (KCl). Whereas, the animal action potential is osmotically neutral because equal amounts of entering sodium and leaving potassium cancel each other osmotically. The interaction of electrical and osmotic relations in plant cells<ref name="Gradmann_1998" group="lower-alpha">{{cite journal | vauthors = Gradmann D, Hoffstadt J | title = Electrocoupling of ion transporters in plants: interaction with internal ion concentrations | journal = The Journal of Membrane Biology | volume = 166 | issue = 1 | pages = 51–9 | date = November 1998 | pmid = 9784585 | doi = 10.1007/s002329900446 | s2cid = 24190001 }}</ref> appears to have arisen from an osmotic function of electrical excitability in a common unicellular ancestors of plants and animals under changing salinity conditions. Further, the present function of rapid signal transmission is seen as a newer accomplishment of [[metazoan]] cells in a more stable osmotic environment.<ref name="Gradmann_1980">

Gradmann, D; Mummert, H in {{harvnb|Spanswick|Lucas|Dainty|1980|loc=''Plant action potentials'', pp. 333–344.}}</ref> It is likely that the familiar signaling function of action potentials in some vascular plants (e.g. ''[[Mimosa pudica]]'') arose independently from that in metazoan excitable cells.

Gradmann, D; Mummert, H in {{harvnb|Spanswick|Lucas|Dainty|1980|loc=''Plant action potentials'', pp. 333–344.}}</ref> It is likely that the familiar signaling function of action potentials in some vascular plants (e.g. ''[[Mimosa pudica]]'') arose independently from that in metazoan excitable cells.

随着随后释放的阳性钾离子，动作电位在植物中涉及盐(KCl)渗透损失。然而，动物的动作电位是渗透中性的，因为等量的钠进入和钾离开相互抵消渗透。植物细胞中电和渗透关系的相互作用似乎起源于盐度变化条件下动植物共同的单细胞祖先的电兴奋渗透作用。此外，目前的快速信号传递功能被认为是后生动物细胞在更稳定的渗透环境中更新的成就。在一些维管植物中，动作电位的常见信号功能可能是。含羞草(Mimosa putica)是独立于后生动物兴奋细胞而产生的。

随着随后释放的阳性钾离子，动作电位在植物中涉及盐(KCl)渗透损失。然而，动物的动作电位是渗透中性的，因为等量的钠进入和钾离开相互抵消渗透。植物细胞s<ref name="Gradmann_1998" group="lower-alpha" />中电和渗透关系的相互作用似乎起源于盐度变化条件下动植物共同的单细胞祖先的电兴奋渗透作用。此外，目前的快速信号传递功能被认为是后生动物细胞在更稳定的渗透环境中更新的成就.<ref name="Gradmann_1980" /> 。在一些维管植物中，动作电位的常见信号功能可能是。含羞草(Mimosa putica)是独立于后生动物兴奋细胞而产生的。

Unlike the rising phase and peak, the falling phase and after-hyperpolarization seem to depend primarily on cations that are not calcium. To initiate repolarization, the cell requires movement of potassium out of the cell through passive transportation on the membrane. This differs from neurons because the movement of potassium does not dominate the decrease in membrane potential; In fact, to fully repolarize, a plant cell requires energy in the form of ATP to assist in the release of hydrogen from the cell – utilizing a transporter commonly known as H+-ATPase.<ref name="Opritov">Opritov, V A, et al. “Direct Coupling of Action Potential Generation in Cells of a Higher Plant (Cucurbita Pepo) with the Operation of an Electrogenic Pump.” ''Russian Journal of Plant Physiology'', vol. 49, no. 1, 2002, pp. 142–147.</ref><ref name=":2" />

Unlike the rising phase and peak, the falling phase and after-hyperpolarization seem to depend primarily on cations that are not calcium. To initiate repolarization, the cell requires movement of potassium out of the cell through passive transportation on the membrane. This differs from neurons because the movement of potassium does not dominate the decrease in membrane potential; In fact, to fully repolarize, a plant cell requires energy in the form of ATP to assist in the release of hydrogen from the cell – utilizing a transporter commonly known as H+-ATPase.<ref name="Opritov">Opritov, V A, et al. “Direct Coupling of Action Potential Generation in Cells of a Higher Plant (Cucurbita Pepo) with the Operation of an Electrogenic Pump.” ''Russian Journal of Plant Physiology'', vol. 49, no. 1, 2002, pp. 142–147.</ref><ref name=":2" />

不同于上升相和峰值，下降相和后超极化似乎主要依赖于不是钙的阳离子。为了启动复极化，细胞需要钾离子通过细胞膜上的被动运输离开细胞。事实上，为了完全再极化，植物细胞需要能量以 ATP 的形式帮助细胞释放氢-利用一种通常被称为 h +-ATP 酶的转运蛋白。奥普里托夫，v a，等。高等植物细胞动作电位的直接耦合与电生泵的运作俄罗斯植物生理学杂志，第一卷。49，不。1,2002，pp.142–147.

不同于上升相和峰值，下降相和后超极化似乎主要依赖于不是钙的阳离子。为了启动复极化，细胞需要钾离子通过细胞膜上的被动运输离开细胞。事实上，为了完全再极化，植物细胞需要能量以 ATP 的形式帮助细胞释放氢-利用一种通常被称为 h +-ATP 酶的转运蛋白。奥普里托夫，v a，等。高等植物细胞动作电位的直接耦合与电生泵的运作俄罗斯植物生理学杂志，第一卷。49，不。1,2002，pp.142–147..<ref name="Opritov" /><ref name=":2" />

= = 在多细胞生物，包括植物、无脊椎动物如昆虫和脊椎动物如爬行动物和哺乳动物中发现了动作电位。海绵似乎是不传递动作电位的多细胞真核生物的主要门类，尽管一些研究表明这些生物也有一种电信号的形式。虽然神经传导速度随轴突直径和髓鞘形成而发生显著变化，但神经静息电位和动作电位的大小和持续时间并没有随着进化而发生很大变化。

==Taxonomic distribution and evolutionary advantages 分类学分布和进化优势==

 

{| class="wikitable" id="action_potential_texonomic_comparison" border="2" cellpadding="5" cellspacing="1" align="center"

{| class="wikitable" id="action_potential_texonomic_comparison" border="2" cellpadding="5" cellspacing="1" align="center"

{| class="wikitable" id="action_potential_texonomic_comparison" border="2" cellpadding="5" cellspacing="1" align="center"

{| class="wikitable" id="action_potential_texonomic_comparison" border="2" cellpadding="5" cellspacing="1" align="center"

|+ Comparison of action potentials (APs) from a representative cross-section of animals

|+Comparison of action potentials (APs) from a representative cross-section of animals动物的代表性横切的动作电位的比较

! Animal !! Cell type !! Resting potential (mV) !! AP increase (mV) !! AP duration (ms) !! Conduction speed (m/s)

! Animal !! Cell type !! Resting potential (mV) !! AP increase (mV) !! AP duration (ms) !! Conduction speed (m/s)

|-

|-

[[Category:Action potentials]]

[[Category:Action potentials]]

[[Category:待整理页面]]

[[Category:待整理页面]]

Given its conservation throughout evolution, the action potential seems to confer evolutionary advantages. One function of action potentials is rapid, long-range signaling within the organism; the conduction velocity can exceed 110&nbsp;m/s, which is one-third the [[speed of sound]]. For comparison, a hormone molecule carried in the bloodstream moves at roughly 8&nbsp;m/s in large arteries. Part of this function is the tight coordination of mechanical events, such as the contraction of the heart. A second function is the computation associated with its generation. Being an all-or-none signal that does not decay with transmission distance, the action potential has similar advantages to [[digital electronics]]. The integration of various dendritic signals at the axon hillock and its thresholding to form a complex train of action potentials is another form of computation, one that has been exploited biologically to form [[central pattern generator]]s and mimicked in [[artificial neural network]]s.

Given its conservation throughout evolution, the action potential seems to confer evolutionary advantages. One function of action potentials is rapid, long-range signaling within the organism; the conduction velocity can exceed 110&nbsp;m/s, which is one-third the [[speed of sound]]. For comparison, a hormone molecule carried in the bloodstream moves at roughly 8&nbsp;m/s in large arteries. Part of this function is the tight coordination of mechanical events, such as the contraction of the heart. A second function is the computation associated with its generation. Being an all-or-none signal that does not decay with transmission distance, the action potential has similar advantages to [[digital electronics]]. The integration of various dendritic signals at the axon hillock and its thresholding to form a complex train of action potentials is another form of computation, one that has been exploited biologically to form [[central pattern generator]]s and mimicked in [[artificial neural network]]s.

鉴于动作电位在整个进化过程中的保守性，它似乎赋予了进化优势。动作电位的一个功能是在生物体内快速的远程信号传导，传导速度可以超过110米/秒，这是声速的三分之一。相比之下，血液中携带的荷尔蒙分子在大动脉中的运动速度大约为每秒8米。这个功能的一部分是机械事件的紧密协调，例如心脏的收缩。第二个函数是与其生成相关的计算。动作电位作为一种全或无信号，不随传输距离衰减，与数字电子技术具有相似的优点。轴突小丘上各种树突信号的整合及其阈值化形成一系列复杂的动作电位是另一种形式的计算方法，这种方法已被生物学方法用来形成中心模式发生器，并在人工神经网络中进行模拟。

鉴于动作电位在整个进化过程中的保守性，它似乎赋予了进化优势。动作电位的一个功能是在生物体内快速的远程信号传导，传导速度可以超过110米/秒，这是声速的三分之一。相比之下，血液中携带的荷尔蒙分子在大动脉中的运动速度大约为每秒8米。这个功能的一部分是机械事件的紧密协调，例如心脏的收缩。第二个函数是与其生成相关的计算。动作电位作为一种全或无信号，不随传输距离衰减，与数字电子技术具有相似的优点。轴突小丘上各种树突信号的整合及其阈值化形成一系列复杂的动作电位是另一种形式的计算方法，这种方法已被生物学方法用来形成中心模式发生器，并在人工神经网络中进行模拟。

The common prokaryotic/eukaryotic ancestor, which lived perhaps four billion years ago, is believed to have had voltage-gated channels. This functionality was likely, at some later point, cross-purposed to provide a communication mechanism. Even modern single-celled bacteria can utilize action potentials to communicate with other bacteria in the same biofilm.<ref>{{cite journal | vauthors = Kristan WB | title = Early evolution of neurons | journal = Current Biology | volume = 26 | issue = 20 | pages = R949–R954 | date = October 2016 | pmid = 27780067 | doi = 10.1016/j.cub.2016.05.030 | doi-access = free }}</ref>

The common prokaryotic/eukaryotic ancestor, which lived perhaps four billion years ago, is believed to have had voltage-gated channels. This functionality was likely, at some later point, cross-purposed to provide a communication mechanism. Even modern single-celled bacteria can utilize action potentials to communicate with other bacteria in the same biofilm.<ref name=":19">{{cite journal | vauthors = Kristan WB | title = Early evolution of neurons | journal = Current Biology | volume = 26 | issue = 20 | pages = R949–R954 | date = October 2016 | pmid = 27780067 | doi = 10.1016/j.cub.2016.05.030 | doi-access = free }}</ref>

生活在大约40亿年前的原核/真核生物的共同祖先，被认为具有电压门控通道。在以后的某个时候，这个功能可能会被用来提供一个通信机制。即使是现代的单细胞细菌也可以利用动作电位与生物膜中的其他细菌进行交流。

生活在大约40亿年前的原核/真核生物的共同祖先，被认为具有电压门控通道。在以后的某个时候，这个功能可能会被用来提供一个通信机制。即使是现代的单细胞细菌也可以利用动作电位与生物膜中的其他细菌进行交流。.<ref name=":19" />

==Experimental methods==

==Experimental methods==

[[Image:Loligo forbesii.jpg|thumb|right|250px|Giant axons of the longfin inshore squid (''[[Doryteuthis pealeii]]'') were [[Marine Biological Laboratory#Neuroscience, neurobiology, and sensory physiology|crucial for scientists]] to understand the action potential.<ref>{{cite book |url=https://books.google.com/books?id=SDi2BQAAQBAJ |title=The Brain, the Nervous System, and Their Diseases |first=Jennifer L. |last=Hellier | name-list-style = vanc |year=2014 |pages=532 |publisher=ABC-Clio |isbn=9781610693387}}</ref>|链接=Special:FilePath/Loligo_forbesii.jpg]]

[[Image:Loligo forbesii.jpg|thumb|right|250px|Giant axons of the longfin inshore squid (''[[Doryteuthis pealeii]]'') were [[Marine Biological Laboratory#Neuroscience, neurobiology, and sensory physiology|crucial for scientists]] to understand the action potential.<ref>{{cite book |url=https://books.google.com/books?id=SDi2BQAAQBAJ |title=The Brain, the Nervous System, and Their Diseases |first=Jennifer L. |last=Hellier | name-list-style = vanc |year=2014 |pages=532 |publisher=ABC-Clio |isbn=9781610693387}}</ref>|链接=Special:FilePath/Loligo_forbesii.jpg]]

The first problem was solved by studying the [[Squid giant axon|giant axons]] found in the neurons of the [[squid]] (''[[Loligo forbesii]]'' and ''[[Doryteuthis pealeii]]'', at the time classified as ''Loligo pealeii'').<ref name="keynes_1989" group="lower-alpha">{{cite journal | vauthors = Keynes RD | title = The role of giant axons in studies of the nerve impulse | journal = BioEssays | volume = 10 | issue = 2–3 | pages = 90–3 | year = 1989 | pmid = 2541698 | doi = 10.1002/bies.950100213 }}</ref> These axons are so large in diameter (roughly 1&nbsp;mm, or 100-fold larger than a typical neuron) that they can be seen with the naked eye, making them easy to extract and manipulate.<ref name="hodgkin_1952" group="lower-alpha" /><ref name="Meunier" group="lower-alpha">{{cite journal | vauthors = Meunier C, Segev I | title = Playing the devil's advocate: is the Hodgkin-Huxley model useful? | journal = Trends in Neurosciences | volume = 25 | issue = 11 | pages = 558–63 | date = November 2002 | pmid = 12392930 | doi = 10.1016/S0166-2236(02)02278-6 | s2cid = 1355280 }}</ref> However, they are not representative of all excitable cells, and numerous other systems with action potentials have been studied.

The first problem was solved by studying the [[Squid giant axon|giant axons]] found in the neurons of the [[squid]] (''[[Loligo forbesii]]'' and ''[[Doryteuthis pealeii]]'', at the time classified as ''Loligo pealeii'').<ref name="keynes_1989" group="lower-alpha">{{cite journal | vauthors = Keynes RD | title = The role of giant axons in studies of the nerve impulse | journal = BioEssays | volume = 10 | issue = 2–3 | pages = 90–3 | year = 1989 | pmid = 2541698 | doi = 10.1002/bies.950100213 }}</ref> These axons are so large in diameter (roughly 1&nbsp;mm, or 100-fold larger than a typical neuron) that they can be seen with the naked eye, making them easy to extract and manipulate.<ref name="hodgkin_1952" group="lower-alpha" /><ref name="Meunier" group="lower-alpha">{{cite journal | vauthors = Meunier C, Segev I | title = Playing the devil's advocate: is the Hodgkin-Huxley model useful? | journal = Trends in Neurosciences | volume = 25 | issue = 11 | pages = 558–63 | date = November 2002 | pmid = 12392930 | doi = 10.1016/S0166-2236(02)02278-6 | s2cid = 1355280 }}</ref> However, they are not representative of all excitable cells, and numerous other systems with action potentials have been studied.

第一个问题通过研究乌贼神经元中发现的巨大轴突(Loligo forbesii 和 Doryteuthis pealeii，当时被归类为 Loligo pealeii)得到了解决。这些轴突直径很大(大约1毫米，比一个典型的神经元大100倍) ，可以用肉眼看到，因此很容易提取和操作。然而，它们并不代表所有可兴奋细胞，许多其他具有动作电位的系统已被研究。

第一个问题通过研究乌贼神经元中发现的巨大轴突(Loligo forbesii 和 Doryteuthis pealeii，当时被归类为 Loligo pealeii)得到了解决.<ref name="keynes_1989" group="lower-alpha" /> 。这些轴突直径很大(大约1毫米，比一个典型的神经元大100倍) ，可以用肉眼看到，因此很容易提取和操作e.<ref name="hodgkin_1952" group="lower-alpha" /><ref name="Meunier" group="lower-alpha" /> 。然而，它们并不代表所有可兴奋细胞，许多其他具有动作电位的系统已被研究。

The second problem was addressed with the crucial development of the [[voltage clamp]],<ref name="cole_1949" group="lower-alpha">{{cite journal | vauthors = Cole KS | year = 1949 | title = Dynamic electrical characteristics of the squid axon membrane | journal = Arch. Sci. Physiol. | volume = 3 | pages = 253–8| author-link = Kenneth Stewart Cole }}</ref> which permitted experimenters to study the ionic currents underlying an action potential in isolation, and eliminated a key source of [[electronic noise]], the current ''I_C'' associated with the [[capacitance]] ''C'' of the membrane.{{sfn|Junge|1981|pp=63–82}} Since the current equals ''C'' times the rate of change of the transmembrane voltage ''V_m'', the solution was to design a circuit that kept ''V_m'' fixed (zero rate of change) regardless of the currents flowing across the membrane. Thus, the current required to keep ''V_m'' at a fixed value is a direct reflection of the current flowing through the membrane. Other electronic advances included the use of [[Faraday cage]]s and electronics with high [[input impedance]], so that the measurement itself did not affect the voltage being measured.{{sfn|Kettenmann|Grantyn|1992}}

The second problem was addressed with the crucial development of the [[voltage clamp]],<ref name="cole_1949" group="lower-alpha">{{cite journal | vauthors = Cole KS | year = 1949 | title = Dynamic electrical characteristics of the squid axon membrane | journal = Arch. Sci. Physiol. | volume = 3 | pages = 253–8| author-link = Kenneth Stewart Cole }}</ref> which permitted experimenters to study the ionic currents underlying an action potential in isolation, and eliminated a key source of [[electronic noise]], the current ''I_C'' associated with the [[capacitance]] ''C'' of the membrane.{{sfn|Junge|1981|pp=63–82}} Since the current equals ''C'' times the rate of change of the transmembrane voltage ''V_m'', the solution was to design a circuit that kept ''V_m'' fixed (zero rate of change) regardless of the currents flowing across the membrane. Thus, the current required to keep ''V_m'' at a fixed value is a direct reflection of the current flowing through the membrane. Other electronic advances included the use of [[Faraday cage]]s and electronics with high [[input impedance]], so that the measurement itself did not affect the voltage being measured.{{sfn|Kettenmann|Grantyn|1992}}

第二个问题是关于电压钳的关键发展，它允许实验者在隔离的情况下研究作用于动作电位的离子电流，并消除了电子噪声的一个关键来源---- 与膜电容 c 相关的电流 IC。由于电流等于 c 乘以跨膜电压 Vm 的变化率，所以解决方案是设计一个电路，使 Vm 保持固定(零变化率) ，而不管跨膜电流的变化。因此，使 Vm 保持在一个固定值所需的电流是流过薄膜的电流的直接反射。其他电子方面的进步包括使用法拉第笼和具有高输入阻抗的电子器件，这样测量本身就不会影响被测量的电压。

第二个问题是关于电压钳,<ref name="cole_1949" group="lower-alpha" /> 的关键发展，它允许实验者在隔离的情况下研究作用于动作电位的离子电流，并消除了电子噪声的一个关键来源---- 与膜电容 c 相关的电流 IC。由于电流等于 c 乘以跨膜电压 Vm 的变化率，所以解决方案是设计一个电路，使 Vm 保持固定(零变化率) ，而不管跨膜电流的变化。因此，使 Vm 保持在一个固定值所需的电流是流过薄膜的电流的直接反射。其他电子方面的进步包括使用法拉第笼和具有高输入阻抗的电子器件，这样测量本身就不会影响被测量的电压。

The third problem, that of obtaining electrodes small enough to record voltages within a single axon without perturbing it, was solved in 1949 with the invention of the glass micropipette electrode,<ref name="ling_1949" group="lower-alpha">{{cite journal | vauthors = Ling G, Gerard RW | title = The normal membrane potential of frog sartorius fibers | journal = Journal of Cellular and Comparative Physiology | volume = 34 | issue = 3 | pages = 383–96 | date = December 1949 | pmid = 15410483 | doi = 10.1002/jcp.1030340304 }}</ref> which was quickly adopted by other researchers.<ref name="nastuk_1950" group="lower-alpha">{{cite journal | vauthors = Nastuk WL, Hodgkin A | year = 1950 | title = The electrical activity of single muscle fibers | journal = Journal of Cellular and Comparative Physiology | volume = 35 | pages = 39–73 | doi = 10.1002/jcp.1030350105 }}</ref><ref name="brock_1952" group="lower-alpha">{{cite journal | vauthors = Brock LG, Coombs JS, Eccles JC | title = The recording of potentials from motoneurones with an intracellular electrode | journal = The Journal of Physiology | volume = 117 | issue = 4 | pages = 431–60 | date = August 1952 | pmid = 12991232 | pmc = 1392415 | doi = 10.1113/jphysiol.1952.sp004759 }}</ref> Refinements of this method are able to produce electrode tips that are as fine as 100 [[Ångström|Å]] (10 [[nanometre|nm]]), which also confers high input impedance.<ref>Snell, FM in {{harvnb|Lavallée|Schanne|Hébert|1969|loc=''Some Electrical Properties of Fine-Tipped Pipette Microelectrodes''.}}</ref> Action potentials may also be recorded with small metal electrodes placed just next to a neuron, with [[neurochip]]s containing [[EOSFET]]s, or optically with dyes that are [[Calcium imaging|sensitive to Ca²⁺]] or to voltage.<ref name="dyes" group="lower-alpha">{{cite journal | vauthors = Ross WN, Salzberg BM, Cohen LB, Davila HV | title = A large change in dye absorption during the action potential | journal = Biophysical Journal | volume = 14 | issue = 12 | pages = 983–6 | date = December 1974 | pmid = 4429774 | pmc = 1334592 | doi = 10.1016/S0006-3495(74)85963-1 | bibcode = 1974BpJ....14..983R }}<br />* {{cite journal | vauthors = Grynkiewicz G, Poenie M, Tsien RY | title = A new generation of Ca2+ indicators with greatly improved fluorescence properties | journal = The Journal of Biological Chemistry | volume = 260 | issue = 6 | pages = 3440–50 | date = March 1985 | doi = 10.1016/S0021-9258(19)83641-4 | pmid = 3838314 | doi-access = free }}</ref>

The third problem, that of obtaining electrodes small enough to record voltages within a single axon without perturbing it, was solved in 1949 with the invention of the glass micropipette electrode,<ref name="ling_1949" group="lower-alpha">{{cite journal | vauthors = Ling G, Gerard RW | title = The normal membrane potential of frog sartorius fibers | journal = Journal of Cellular and Comparative Physiology | volume = 34 | issue = 3 | pages = 383–96 | date = December 1949 | pmid = 15410483 | doi = 10.1002/jcp.1030340304 }}</ref> which was quickly adopted by other researchers.<ref name="nastuk_1950" group="lower-alpha">{{cite journal | vauthors = Nastuk WL, Hodgkin A | year = 1950 | title = The electrical activity of single muscle fibers | journal = Journal of Cellular and Comparative Physiology | volume = 35 | pages = 39–73 | doi = 10.1002/jcp.1030350105 }}</ref><ref name="brock_1952" group="lower-alpha">{{cite journal | vauthors = Brock LG, Coombs JS, Eccles JC | title = The recording of potentials from motoneurones with an intracellular electrode | journal = The Journal of Physiology | volume = 117 | issue = 4 | pages = 431–60 | date = August 1952 | pmid = 12991232 | pmc = 1392415 | doi = 10.1113/jphysiol.1952.sp004759 }}</ref> Refinements of this method are able to produce electrode tips that are as fine as 100 [[Ångström|Å]] (10 [[nanometre|nm]]), which also confers high input impedance.<ref name=":20">Snell, FM in {{harvnb|Lavallée|Schanne|Hébert|1969|loc=''Some Electrical Properties of Fine-Tipped Pipette Microelectrodes''.}}</ref> Action potentials may also be recorded with small metal electrodes placed just next to a neuron, with [[neurochip]]s containing [[EOSFET]]s, or optically with dyes that are [[Calcium imaging|sensitive to Ca²⁺]] or to voltage.<ref name="dyes" group="lower-alpha">{{cite journal | vauthors = Ross WN, Salzberg BM, Cohen LB, Davila HV | title = A large change in dye absorption during the action potential | journal = Biophysical Journal | volume = 14 | issue = 12 | pages = 983–6 | date = December 1974 | pmid = 4429774 | pmc = 1334592 | doi = 10.1016/S0006-3495(74)85963-1 | bibcode = 1974BpJ....14..983R }}<br />* {{cite journal | vauthors = Grynkiewicz G, Poenie M, Tsien RY | title = A new generation of Ca2+ indicators with greatly improved fluorescence properties | journal = The Journal of Biological Chemistry | volume = 260 | issue = 6 | pages = 3440–50 | date = March 1985 | doi = 10.1016/S0021-9258(19)83641-4 | pmid = 3838314 | doi-access = free }}</ref>

<nowiki>*</nowiki>  

第三个问题是如何获得足够小的电极来记录单个轴突内的电压而不对其造成干扰，这个问题在1949年由于玻璃微移液管电极,<ref name="ling_1949" group="lower-alpha" /> 的发明而得到解决，并且很快被其他研究人员采用.<ref name="nastuk_1950" group="lower-alpha" /><ref name="brock_1952" group="lower-alpha" /> 。这种方法的改进可以生产出100纳米的电极尖端，同时也提供了高的输入阻抗.<ref name=":20" /> 。动作电位中的 Snell 和 FM 也可以用放置在神经元旁的小金属电极记录下来，用含有 eosfet 的神经芯片，或者用对 Ca < sup > 2 +  或电压敏感的染料记录下来。.<ref name="dyes" group="lower-alpha" />< br/> *  

 

第三个问题是如何获得足够小的电极来记录单个轴突内的电压而不对其造成干扰，这个问题在1949年由于玻璃微移液管电极的发明而得到解决，并且很快被其他研究人员采用。这种方法的改进可以生产出100纳米的电极尖端，同时也提供了高的输入阻抗。动作电位中的 Snell 和 FM 也可以用放置在神经元旁的小金属电极记录下来，用含有 eosfet 的神经芯片，或者用对 Ca < sup > 2 +  或电压敏感的染料记录下来。< br/> *  

[[Image:Single channel.png|thumb|left|As revealed by a [[patch clamp]] electrode, an [[ion channel]] has two states: open (high conductance) and closed (low conductance).|链接=Special:FilePath/Single_channel.png]]

[[Image:Single channel.png|thumb|left|As revealed by a [[patch clamp]] electrode, an [[ion channel]] has two states: open (high conductance) and closed (low conductance).|链接=Special:FilePath/Single_channel.png]]

While glass micropipette electrodes measure the sum of the currents passing through many ion channels, studying the electrical properties of a single ion channel became possible in the 1970s with the development of the [[patch clamp]] by [[Erwin Neher]] and [[Bert Sakmann]]. For this discovery, they were awarded the [[Nobel Prize in Physiology or Medicine]] in 1991.<ref name="Nobel_1991" group="lower-Greek">{{cite press release | url = http://nobelprize.org/nobel_prizes/medicine/laureates/1991/press.html | title = The Nobel Prize in Physiology or Medicine 1991 | publisher = The Royal Swedish Academy of Science | year = 1991 | access-date = 2010-02-21 | url-status = live | archive-url = https://web.archive.org/web/20100324031907/http://nobelprize.org/nobel_prizes/medicine/laureates/1991/press.html | archive-date = 24 March 2010 | df = dmy-all }}</ref> Patch-clamping verified that ionic channels have discrete states of conductance, such as open, closed and inactivated.

While glass micropipette electrodes measure the sum of the currents passing through many ion channels, studying the electrical properties of a single ion channel became possible in the 1970s with the development of the [[patch clamp]] by [[Erwin Neher]] and [[Bert Sakmann]]. For this discovery, they were awarded the [[Nobel Prize in Physiology or Medicine]] in 1991.<ref name="Nobel_1991" group="lower-Greek">{{cite press release | url = http://nobelprize.org/nobel_prizes/medicine/laureates/1991/press.html | title = The Nobel Prize in Physiology or Medicine 1991 | publisher = The Royal Swedish Academy of Science | year = 1991 | access-date = 2010-02-21 | url-status = live | archive-url = https://web.archive.org/web/20100324031907/http://nobelprize.org/nobel_prizes/medicine/laureates/1991/press.html | archive-date = 24 March 2010 | df = dmy-all }}</ref> Patch-clamping verified that ionic channels have discrete states of conductance, such as open, closed and inactivated.

玻璃微吸管电极测量通过许多离子通道的电流总和，研究单个离子通道的电学性质在20世纪70年代埃尔温 · 内尔和伯特 · 萨克曼发明的膜片钳成为可能。由于这一发现，他们在1991年被授予诺贝尔生理学或医学奖科学奖。膜片钳技术证实了离子通道具有分立的电导状态，如开放状态、闭合状态和失活状态。

玻璃微吸管电极测量通过许多离子通道的电流总和，研究单个离子通道的电学性质在20世纪70年代埃尔温 · 内尔和伯特 · 萨克曼发明的膜片钳成为可能。由于这一发现，他们在1991年被授予诺贝尔生理学或医学奖科学奖.<ref name="Nobel_1991" group="lower-Greek" />。膜片钳技术证实了离子通道具有分立的电导状态，如开放状态、闭合状态和失活状态。

[[Optical imaging]] technologies have been developed in recent years to measure action potentials, either via simultaneous multisite recordings or with ultra-spatial resolution. Using [[Potentiometric dyes|voltage-sensitive dyes]], action potentials have been optically recorded from a tiny patch of [[cardiomyocyte]] membrane.<ref name="pmid19289075" group="lower-alpha">{{cite journal | vauthors = Bu G, Adams H, Berbari EJ, Rubart M | title = Uniform action potential repolarization within the sarcolemma of in situ ventricular cardiomyocytes | journal = Biophysical Journal | volume = 96 | issue = 6 | pages = 2532–46 | date = March 2009 | pmid = 19289075 | pmc = 2907679 | doi = 10.1016/j.bpj.2008.12.3896 | bibcode = 2009BpJ....96.2532B }}</ref>

[[Optical imaging]] technologies have been developed in recent years to measure action potentials, either via simultaneous multisite recordings or with ultra-spatial resolution. Using [[Potentiometric dyes|voltage-sensitive dyes]], action potentials have been optically recorded from a tiny patch of [[cardiomyocyte]] membrane.<ref name="pmid19289075" group="lower-alpha">{{cite journal | vauthors = Bu G, Adams H, Berbari EJ, Rubart M | title = Uniform action potential repolarization within the sarcolemma of in situ ventricular cardiomyocytes | journal = Biophysical Journal | volume = 96 | issue = 6 | pages = 2532–46 | date = March 2009 | pmid = 19289075 | pmc = 2907679 | doi = 10.1016/j.bpj.2008.12.3896 | bibcode = 2009BpJ....96.2532B }}</ref>

==Neurotoxins==

==Neurotoxins==

一些天然和人工的神经毒素被设计用来阻断动作电位。来自河豚的河豚毒素和来自沟鞭藻属的石房蛤毒素通过抑制电压敏感性钠通道来阻断动作电位; 同样地，黑曼巴蛇的树眼镜蛇毒素也会抑制电压敏感性钾离子通道。这种离子通道的抑制剂有一个重要的研究目的，它可以让科学家随意关闭特定的通道，从而分离出其他通道的贡献; 它们也可以用亲和色谱法来净化离子通道或测定它们的浓度。然而，这些抑制剂也能产生有效的神经毒素，并被认为是化学武器。针对昆虫离子通道的神经毒素一直是有效的杀虫剂，其中一个例子是合成氯菊酯，它延长了与动作电位有关的钠通道的激活。昆虫的离子通道与人类的离子通道完全不同，因此对人类几乎没有副作用。

一些天然和人工的神经毒素被设计用来阻断动作电位。来自河豚的河豚毒素和来自沟鞭藻属的石房蛤毒素通过抑制电压敏感性钠通道来阻断动作电位; 同样地，黑曼巴蛇的树眼镜蛇毒素也会抑制电压敏感性钾离子通道。这种离子通道的抑制剂有一个重要的研究目的，它可以让科学家随意关闭特定的通道，从而分离出其他通道的贡献; 它们也可以用亲和色谱法来净化离子通道或测定它们的浓度。然而，这些抑制剂也能产生有效的神经毒素，并被认为是化学武器。针对昆虫离子通道的神经毒素一直是有效的杀虫剂，其中一个例子是合成氯菊酯，它延长了与动作电位有关的钠通道的激活。昆虫的离子通道与人类的离子通道完全不同，因此对人类几乎没有副作用。

==History==

==History历史==

[[Image:PurkinjeCell.jpg|thumb|left|Image of two [[Purkinje cell]]s (labeled as '''A''') drawn by [[Santiago Ramón y Cajal]] in 1899. Large trees of [[dendrite]]s feed into the [[soma (biology)|soma]], from which a single [[axon]] emerges and moves generally downwards with a few branch points. The smaller cells labeled '''B''' are [[granule cell]]s.|alt=Hand drawn figure of two Purkinje cells side by side with dendrites projecting upwards that look like tree branches and a few axons projected downwards that connect to a few granule cells at the bottom of the drawing.]]

[[Image:PurkinjeCell.jpg|thumb|left|Image of two [[Purkinje cell]]s (labeled as '''A''') drawn by [[Santiago Ramón y Cajal]] in 1899. Large trees of [[dendrite]]s feed into the [[soma (biology)|soma]], from which a single [[axon]] emerges and moves generally downwards with a few branch points. The smaller cells labeled '''B''' are [[granule cell]]s.|alt=Hand drawn figure of two Purkinje cells side by side with dendrites projecting upwards that look like tree branches and a few axons projected downwards that connect to a few granule cells at the bottom of the drawing.]]

The role of electricity in the nervous systems of animals was first observed in dissected [[frog]]s by [[Luigi Galvani]], who studied it from 1791 to 1797.<ref name="piccolino_1997" group="lower-alpha">{{cite journal | vauthors = Piccolino M | title = Luigi Galvani and animal electricity: two centuries after the foundation of electrophysiology | journal = Trends in Neurosciences | volume = 20 | issue = 10 | pages = 443–8 | date = October 1997 | pmid = 9347609 | doi = 10.1016/S0166-2236(97)01101-6 | s2cid = 23394494 }}</ref> Galvani's results stimulated [[Alessandro Volta]] to develop the [[Voltaic pile]]—the earliest-known [[battery (electricity)|electric battery]]—with which he studied animal electricity (such as [[electric eel]]s) and the physiological responses to applied [[direct current|direct-current]] [[voltage]]s.<ref name="piccolino_2000" group="lower-alpha">{{cite journal | vauthors = Piccolino M | title = The bicentennial of the Voltaic battery (1800-2000): the artificial electric organ | journal = Trends in Neurosciences | volume = 23 | issue = 4 | pages = 147–51 | date = April 2000 | pmid = 10717671 | doi = 10.1016/S0166-2236(99)01544-1 | s2cid = 393323 }}</ref>

The role of electricity in the nervous systems of animals was first observed in dissected [[frog]]s by [[Luigi Galvani]], who studied it from 1791 to 1797.<ref name="piccolino_1997" group="lower-alpha">{{cite journal | vauthors = Piccolino M | title = Luigi Galvani and animal electricity: two centuries after the foundation of electrophysiology | journal = Trends in Neurosciences | volume = 20 | issue = 10 | pages = 443–8 | date = October 1997 | pmid = 9347609 | doi = 10.1016/S0166-2236(97)01101-6 | s2cid = 23394494 }}</ref> Galvani's results stimulated [[Alessandro Volta]] to develop the [[Voltaic pile]]—the earliest-known [[battery (electricity)|electric battery]]—with which he studied animal electricity (such as [[electric eel]]s) and the physiological responses to applied [[direct current|direct-current]] [[voltage]]s.<ref name="piccolino_2000" group="lower-alpha">{{cite journal | vauthors = Piccolino M | title = The bicentennial of the Voltaic battery (1800-2000): the artificial electric organ | journal = Trends in Neurosciences | volume = 23 | issue = 4 | pages = 147–51 | date = April 2000 | pmid = 10717671 | doi = 10.1016/S0166-2236(99)01544-1 | s2cid = 393323 }}</ref>

电在动物神经系统中的作用最早是由路易吉 · 伽伐尼在解剖的青蛙中观察到的，他从1791年到1797年研究了这一现象。伽伐尼的研究结果激发了亚历山德罗·伏特发明了伏打电堆ーー已知最早的电池ーー他用这种电池研究了动物电(如电鳗)以及对直流电压的生理反应。

电在动物神经系统中的作用最早是由 Luigi Galvani 在解剖的青蛙中观察到的，他从1791年到1797年研究了这一现象。伽伐尼的研究结果激发了亚历山德罗·伏特发明了伏打电堆ーー已知最早的电池ーー他用这种电池研究了动物电(如电鳗)以及对直流电压的生理反应.<ref name="piccolino_2000" group="lower-alpha" />。

Scientists of the 19th century studied the propagation of electrical signals in whole [[nerve]]s (i.e., bundles of [[neuron]]s) and demonstrated that nervous tissue was made up of [[cell (biology)|cells]], instead of an interconnected network of tubes (a ''reticulum'').{{sfnm|1a1=Brazier|1y=1961|2a1=McHenry|2a2=Garrison|2y=1969|3a1=Worden|3a2=Swazey|3a3=Adelman|3y=1975}} [[Carlo Matteucci]] followed up Galvani's studies and demonstrated that [[cell membrane]]s had a voltage across them and could produce [[direct current]]. Matteucci's work inspired the German physiologist, [[Emil du Bois-Reymond]], who discovered the action potential in 1843.<ref>{{Cite book|title=Emil du Bois-Reymond : neuroscience, self, and society in nineteenth-century Germany|last=Finkelstein | first = Gabriel Ward | name-list-style = vanc |isbn=9781461950325|location=Cambridge, Massachusetts|oclc=864592470|year = 2013}}</ref> The [[conduction velocity]] of action potentials was first measured in 1850 by du Bois-Reymond's friend, [[Hermann von Helmholtz]].<ref>[[Kathryn Olesko|Olesko, Kathryn M.]], and Frederic L. Holmes. "Experiment, Quantification and Discovery: Helmholtz's Early Physiological Researches, 1843-50". In ''Hermann von Helmholtz and the Foundations of Nineteenth Century Science'', ed. David Cahan, 50-108. Berkeley; Los Angeles; London: University of California, 1994.</ref> To establish that nervous tissue is made up of discrete cells, the Spanish physician [[Santiago Ramón y Cajal]] and his students used a stain developed by [[Camillo Golgi]] to reveal the myriad shapes of neurons, which they rendered painstakingly. For their discoveries, Golgi and Ramón y Cajal were awarded the 1906 [[Nobel Prize in Physiology or Medicine|Nobel Prize in Physiology]].<ref name="Nobel_1906" group="lower-Greek">{{cite press release | url = http://nobelprize.org/medicine/laureates/1906/index.html | title = The Nobel Prize in Physiology or Medicine 1906 | publisher = The Royal Swedish Academy of Science | year = 1906 | access-date = 2010-02-21 | url-status = live | archive-url = https://web.archive.org/web/20081204190959/http://nobelprize.org/medicine/laureates/1906/index.html | archive-date = 4 December 2008 | df = dmy-all }}</ref> Their work resolved a long-standing controversy in the [[neuroanatomy]] of the 19th century; Golgi himself had argued for the network model of the nervous system.

Scientists of the 19th century studied the propagation of electrical signals in whole [[nerve]]s (i.e., bundles of [[neuron]]s) and demonstrated that nervous tissue was made up of [[cell (biology)|cells]], instead of an interconnected network of tubes (a ''reticulum'').{{sfnm|1a1=Brazier|1y=1961|2a1=McHenry|2a2=Garrison|2y=1969|3a1=Worden|3a2=Swazey|3a3=Adelman|3y=1975}} [[Carlo Matteucci]] followed up Galvani's studies and demonstrated that [[cell membrane]]s had a voltage across them and could produce [[direct current]]. Matteucci's work inspired the German physiologist, [[Emil du Bois-Reymond]], who discovered the action potential in 1843.<ref name=":21">{{Cite book|title=Emil du Bois-Reymond : neuroscience, self, and society in nineteenth-century Germany|last=Finkelstein | first = Gabriel Ward | name-list-style = vanc |isbn=9781461950325|location=Cambridge, Massachusetts|oclc=864592470|year = 2013}}</ref> The [[conduction velocity]] of action potentials was first measured in 1850 by du Bois-Reymond's friend, [[Hermann von Helmholtz]].<ref name=":22">[[Kathryn Olesko|Olesko, Kathryn M.]], and Frederic L. Holmes. "Experiment, Quantification and Discovery: Helmholtz's Early Physiological Researches, 1843-50". In ''Hermann von Helmholtz and the Foundations of Nineteenth Century Science'', ed. David Cahan, 50-108. Berkeley; Los Angeles; London: University of California, 1994.</ref> To establish that nervous tissue is made up of discrete cells, the Spanish physician [[Santiago Ramón y Cajal]] and his students used a stain developed by [[Camillo Golgi]] to reveal the myriad shapes of neurons, which they rendered painstakingly. For their discoveries, Golgi and Ramón y Cajal were awarded the 1906 [[Nobel Prize in Physiology or Medicine|Nobel Prize in Physiology]].<ref name="Nobel_1906" group="lower-Greek">{{cite press release | url = http://nobelprize.org/medicine/laureates/1906/index.html | title = The Nobel Prize in Physiology or Medicine 1906 | publisher = The Royal Swedish Academy of Science | year = 1906 | access-date = 2010-02-21 | url-status = live | archive-url = https://web.archive.org/web/20081204190959/http://nobelprize.org/medicine/laureates/1906/index.html | archive-date = 4 December 2008 | df = dmy-all }}</ref> Their work resolved a long-standing controversy in the [[neuroanatomy]] of the 19th century; Golgi himself had argued for the network model of the nervous system.

19世纪的科学家研究了电信号在整个神经(即神经元束)中的传播，并证明神经组织是由细胞组成的，而不是一个互相连接的管网(网状结构)。卡洛 · 马特乌奇继续伽伐尼的研究，证明细胞膜上有一个电压，可以产生直流电。马特乌奇的工作启发了德国生理学家埃米尔 · 杜 · 布瓦-雷蒙德，后者在1843年发现了动作电位。动作电位的传导速度最早是在1850年由杜波依斯-雷蒙德的朋友赫尔曼·冯·亥姆霍兹 · 雷蒙德测量的。凯瑟琳 · m · 奥列斯科和弗雷德里克 · l · 福尔摩斯。“实验、量化与发现: 亥姆霍兹早期生理学研究，1843-50”。在《赫尔曼·冯·亥姆霍兹和19世纪科学的基础》 ，ed。大卫 · 卡汉，50-108。伯克利; 洛杉矶; 伦敦: 加州大学，1994年。为了证明神经组织是由离散的细胞组成的，西班牙物理学家圣地亚哥·拉蒙-卡哈尔和他的学生们使用了 Camillo Golgi 开发的染色剂来显示神经元的无数形状，他们煞费苦心地进行了渲染。由于他们的发现，高尔基和拉蒙 · 卡哈尔获得了1906年的诺贝尔生理学奖。他们的工作解决了19世纪神经解剖学中长期存在的争议; 高尔基自己则主张神经系统的网络模型。

19世纪的科学家研究了电信号在整个神经(即神经元束)中的传播，并证明神经组织是由细胞组成的，而不是一个互相连接的管网(网状结构)。卡洛 · 马特乌奇继续伽伐尼的研究，证明细胞膜上有一个电压，可以产生直流电。马特乌奇的工作启发了德国生理学家埃米尔 · 杜 · 布瓦-雷蒙德，后者在1843年发现了动作电位.<ref name=":21" /> 。动作电位的传导速度最早是在1850年由杜波依斯-雷蒙德的朋友赫尔曼·冯·亥姆霍兹 · 雷蒙德测量的.<ref name=":22" /> T。凯瑟琳 · m · 奥列斯科和弗雷德里克 · l · 福尔摩斯。“实验、量化与发现: 亥姆霍兹早期生理学研究，1843-50”。在《赫尔曼·冯·亥姆霍兹和19世纪科学的基础》 ，ed。大卫 · 卡汉，50-108。伯克利; 洛杉矶; 伦敦: 加州大学，1994年。为了证明神经组织是由离散的细胞组成的，西班牙物理学家圣地亚哥·拉蒙-卡哈尔和他的学生们使用了 Camillo Golgi 开发的染色剂来显示神经元的无数形状，他们煞费苦心地进行了渲染。由于他们的发现，高尔基和拉蒙 · 卡哈尔获得了1906年的诺贝尔生理学奖.<ref name="Nobel_1906" group="lower-Greek" /> 。他们的工作解决了19世纪神经解剖学中长期存在的争议; 高尔基自己则主张神经系统的网络模型。

[[Image:3b8e.png|thumb|right|[[Ribbon diagram]] of the sodium–potassium pump in its E2-Pi state. The estimated boundaries of the [[lipid bilayer]] are shown as blue (intracellular) and red (extracellular) planes.|链接=Special:FilePath/3b8e.png]]

[[Image:3b8e.png|thumb|right|[[Ribbon diagram]] of the sodium–potassium pump in its E2-Pi state. The estimated boundaries of the [[lipid bilayer]] are shown as blue (intracellular) and red (extracellular) planes.|链接=Special:FilePath/3b8e.png]]

The 20th century was a significant era for electrophysiology. In 1902 and again in 1912, [[Julius Bernstein]] advanced the hypothesis that the action potential resulted from a change in the [[permeation|permeability]] of the axonal membrane to ions.<ref name="bernstein_1902_1912" group="lower-alpha">{{cite journal | vauthors = Bernstein J | year = 1902 | title = Untersuchungen zur Thermodynamik der bioelektrischen Ströme | journal = Pflügers Archiv für die gesamte Physiologie | volume = 92 | pages = 521–562 | doi = 10.1007/BF01790181 | issue = 10–12| s2cid = 33229139 | author-link = Julius Bernstein | url = https://zenodo.org/record/2192363 }}</ref>{{sfn|Bernstein|1912}} Bernstein's hypothesis was confirmed by [[Kenneth Stewart Cole|Ken Cole]] and Howard Curtis, who showed that membrane conductance increases during an action potential.<ref group="lower-alpha">{{cite journal | vauthors = Cole KS, Curtis HJ | title = Electric Impedance of the Squid Giant Axon During Activity | journal = The Journal of General Physiology | volume = 22 | issue = 5 | pages = 649–70 | date = May 1939 | pmid = 19873125 | pmc = 2142006 | doi = 10.1085/jgp.22.5.649 | author-link1 = Kenneth Stewart Cole }}</ref> In 1907, [[Louis Lapicque]] suggested that the action potential was generated as a threshold was crossed,<ref group="lower-alpha">{{cite journal | vauthors = Lapicque L | year = 1907 | title = Recherches quantitatives sur l'excitationelectrique des nerfs traitee comme une polarisation | journal = J. Physiol. Pathol. Gen | volume = 9| pages = 620–635 }}</ref> what would be later shown as a product of the [[dynamical system]]s of ionic conductances. In 1949, [[Alan Lloyd Hodgkin|Alan Hodgkin]] and [[Bernard Katz]] refined Bernstein's hypothesis by considering that the axonal membrane might have different permeabilities to different ions; in particular, they demonstrated the crucial role of the sodium permeability for the action potential.<ref name="hodgkin_1949" group="lower-alpha">{{cite journal | vauthors = Hodgkin AL, Katz B | title = The effect of sodium ions on the electrical activity of giant axon of the squid | journal = The Journal of Physiology | volume = 108 | issue = 1 | pages = 37–77 | date = March 1949 | pmid = 18128147 | pmc = 1392331 | doi = 10.1113/jphysiol.1949.sp004310 | author-link1 = Alan Lloyd Hodgkin | author-link2 = Bernard Katz }}</ref> They made the first actual recording of the electrical changes across the neuronal membrane that mediate the action potential.<ref group="lower-Greek">{{cite journal |last=Warlow|first=Charles| name-list-style = vanc |title=The Recent Evolution of a Symbiotic Ion Channel in the Legume Family Altered Ion Conductance and Improved Functionality in Calcium Signaling|journal=Practical Neurology|volume=7|issue=3|pages=192–197|url=http://pn.bmj.com/content/7/3/192.full|publisher=BMJ Publishing Group|access-date=23 March 2013|url-status=live|archive-url=https://web.archive.org/web/20120314104408/http://pn.bmj.com/content/7/3/192.full|archive-date=14 March 2012|df=dmy-all|date=June 2007}}</ref> This line of research culminated in the five 1952 papers of Hodgkin, Katz and [[Andrew Huxley]], in which they applied the [[voltage clamp]] technique to determine the dependence of the axonal membrane's permeabilities to sodium and potassium ions on voltage and time, from which they were able to reconstruct the action potential quantitatively.<ref name="hodgkin_1952" group="lower-alpha" /> Hodgkin and Huxley correlated the properties of their mathematical model with discrete [[ion channel]]s that could exist in several different states, including "open", "closed", and "inactivated". Their hypotheses were confirmed in the mid-1970s and 1980s by [[Erwin Neher]] and [[Bert Sakmann]], who developed the technique of [[patch clamp]]ing to examine the conductance states of individual ion channels.<ref name="patch_clamp" group="lower-alpha">{{cite journal | vauthors = Neher E, Sakmann B | title = Single-channel currents recorded from membrane of denervated frog muscle fibres | journal = Nature | volume = 260 | issue = 5554 | pages = 799–802 | date = April 1976 | pmid = 1083489 | doi = 10.1038/260799a0 | author-link1 = Erwin Neher | bibcode = 1976Natur.260..799N | s2cid = 4204985 }}<br />* {{cite journal | vauthors = Hamill OP, Marty A, Neher E, Sakmann B, Sigworth FJ | title = Improved patch-clamp techniques for high-resolution current recording from cells and cell-free membrane patches | journal = Pflügers Archiv | volume = 391 | issue = 2 | pages = 85–100 | date = August 1981 | pmid = 6270629 | doi = 10.1007/BF00656997 | s2cid = 12014433 }}<br />* {{cite journal | vauthors = Neher E, Sakmann B | title = The patch clamp technique | journal = Scientific American | volume = 266 | issue = 3 | pages = 44–51 | date = March 1992 | pmid = 1374932 | doi = 10.1038/scientificamerican0392-44 | author-link1 = Erwin Neher | bibcode = 1992SciAm.266c..44N }}</ref> In the 21st century, researchers are beginning to understand the structural basis for these conductance states and for the selectivity of channels for their species of ion,<ref name="yellen_2002" group="lower-alpha">{{cite journal | vauthors = Yellen G | title = The voltage-gated potassium channels and their relatives | journal = Nature | volume = 419 | issue = 6902 | pages = 35–42 | date = September 2002 | pmid = 12214225 | doi = 10.1038/nature00978 | bibcode = 2002Natur.419...35Y | s2cid = 4420877 }}</ref> through the atomic-resolution [[X-ray crystallography|crystal structures]],<ref name="doyle_1998" group="lower-alpha">{{cite journal | vauthors = Doyle DA, Morais Cabral J, Pfuetzner RA, Kuo A, Gulbis JM, Cohen SL, Chait BT, MacKinnon R | display-authors = 6 | title = The structure of the potassium channel: molecular basis of K+ conduction and selectivity | journal = Science | volume = 280 | issue = 5360 | pages = 69–77 | date = April 1998 | pmid = 9525859 | doi = 10.1126/science.280.5360.69 | bibcode = 1998Sci...280...69D }}<br />* {{cite journal | vauthors = Zhou Y, Morais-Cabral JH, Kaufman A, MacKinnon R | title = Chemistry of ion coordination and hydration revealed by a K+ channel-Fab complex at 2.0 A resolution | journal = Nature | volume = 414 | issue = 6859 | pages = 43–8 | date = November 2001 | pmid = 11689936 | doi = 10.1038/35102009 | bibcode = 2001Natur.414...43Z | s2cid = 205022645 }}<br />* {{cite journal | vauthors = Jiang Y, Lee A, Chen J, Ruta V, Cadene M, Chait BT, MacKinnon R | title = X-ray structure of a voltage-dependent K+ channel | journal = Nature | volume = 423 | issue = 6935 | pages = 33–41 | date = May 2003 | pmid = 12721618 | doi = 10.1038/nature01580 | bibcode = 2003Natur.423...33J | s2cid = 4347957 }}</ref> fluorescence distance measurements<ref name="FRET" group="lower-alpha">{{cite journal | vauthors = Cha A, Snyder GE, Selvin PR, Bezanilla F | title = Atomic scale movement of the voltage-sensing region in a potassium channel measured via spectroscopy | journal = Nature | volume = 402 | issue = 6763 | pages = 809–13 | date = December 1999 | pmid = 10617201 | doi = 10.1038/45552 | bibcode = 1999Natur.402..809C | s2cid = 4353978 }}<br />* {{cite journal | vauthors = Glauner KS, Mannuzzu LM, Gandhi CS, Isacoff EY | title = Spectroscopic mapping of voltage sensor movement in the Shaker potassium channel | journal = Nature | volume = 402 | issue = 6763 | pages = 813–7 | date = December 1999 | pmid = 10617202 | doi = 10.1038/45561 | bibcode = 1999Natur.402..813G | s2cid = 4417476 }}<br />* {{cite journal | vauthors = Bezanilla F | title = The voltage sensor in voltage-dependent ion channels | journal = Physiological Reviews | volume = 80 | issue = 2 | pages = 555–92 | date = April 2000 | pmid = 10747201 | doi = 10.1152/physrev.2000.80.2.555 }}</ref> and [[cryo-electron microscopy]] studies.<ref name="cryoEM" group="lower-alpha">{{cite journal | vauthors = Catterall WA | title = A 3D view of sodium channels | journal = Nature | volume = 409 | issue = 6823 | pages = 988–9, 991 | date = February 2001 | pmid = 11234048 | doi = 10.1038/35059188 | bibcode = 2001Natur.409..988C | s2cid = 4371677 | doi-access = free }}<br />* {{cite journal | vauthors = Sato C, Ueno Y, Asai K, Takahashi K, Sato M, Engel A, Fujiyoshi Y | title = The voltage-sensitive sodium channel is a bell-shaped molecule with several cavities | journal = Nature | volume = 409 | issue = 6823 | pages = 1047–51 | date = February 2001 | pmid = 11234014 | doi = 10.1038/35059098 | bibcode = 2001Natur.409.1047S | s2cid = 4430165 }}</ref>

The 20th century was a significant era for electrophysiology. In 1902 and again in 1912, [[Julius Bernstein]] advanced the hypothesis that the action potential resulted from a change in the [[permeation|permeability]] of the axonal membrane to ions.<ref name="bernstein_1902_1912" group="lower-alpha">{{cite journal | vauthors = Bernstein J | year = 1902 | title = Untersuchungen zur Thermodynamik der bioelektrischen Ströme | journal = Pflügers Archiv für die gesamte Physiologie | volume = 92 | pages = 521–562 | doi = 10.1007/BF01790181 | issue = 10–12| s2cid = 33229139 | author-link = Julius Bernstein | url = https://zenodo.org/record/2192363 }}</ref>{{sfn|Bernstein|1912}} Bernstein's hypothesis was confirmed by [[Kenneth Stewart Cole|Ken Cole]] and Howard Curtis, who showed that membrane conductance increases during an action potential.<ref group="lower-alpha" name=":16">{{cite journal | vauthors = Cole KS, Curtis HJ | title = Electric Impedance of the Squid Giant Axon During Activity | journal = The Journal of General Physiology | volume = 22 | issue = 5 | pages = 649–70 | date = May 1939 | pmid = 19873125 | pmc = 2142006 | doi = 10.1085/jgp.22.5.649 | author-link1 = Kenneth Stewart Cole }}</ref> In 1907, [[Louis Lapicque]] suggested that the action potential was generated as a threshold was crossed,<ref group="lower-alpha" name=":17">{{cite journal | vauthors = Lapicque L | year = 1907 | title = Recherches quantitatives sur l'excitationelectrique des nerfs traitee comme une polarisation | journal = J. Physiol. Pathol. Gen | volume = 9| pages = 620–635 }}</ref> what would be later shown as a product of the [[dynamical system]]s of ionic conductances. In 1949, [[Alan Lloyd Hodgkin|Alan Hodgkin]] and [[Bernard Katz]] refined Bernstein's hypothesis by considering that the axonal membrane might have different permeabilities to different ions; in particular, they demonstrated the crucial role of the sodium permeability for the action potential.<ref name="hodgkin_1949" group="lower-alpha">{{cite journal | vauthors = Hodgkin AL, Katz B | title = The effect of sodium ions on the electrical activity of giant axon of the squid | journal = The Journal of Physiology | volume = 108 | issue = 1 | pages = 37–77 | date = March 1949 | pmid = 18128147 | pmc = 1392331 | doi = 10.1113/jphysiol.1949.sp004310 | author-link1 = Alan Lloyd Hodgkin | author-link2 = Bernard Katz }}</ref> They made the first actual recording of the electrical changes across the neuronal membrane that mediate the action potential.<ref group="lower-Greek" name=":0">{{cite journal |last=Warlow|first=Charles| name-list-style = vanc |title=The Recent Evolution of a Symbiotic Ion Channel in the Legume Family Altered Ion Conductance and Improved Functionality in Calcium Signaling|journal=Practical Neurology|volume=7|issue=3|pages=192–197|url=http://pn.bmj.com/content/7/3/192.full|publisher=BMJ Publishing Group|access-date=23 March 2013|url-status=live|archive-url=https://web.archive.org/web/20120314104408/http://pn.bmj.com/content/7/3/192.full|archive-date=14 March 2012|df=dmy-all|date=June 2007}}</ref> This line of research culminated in the five 1952 papers of Hodgkin, Katz and [[Andrew Huxley]], in which they applied the [[voltage clamp]] technique to determine the dependence of the axonal membrane's permeabilities to sodium and potassium ions on voltage and time, from which they were able to reconstruct the action potential quantitatively.<ref name="hodgkin_1952" group="lower-alpha" /> Hodgkin and Huxley correlated the properties of their mathematical model with discrete [[ion channel]]s that could exist in several different states, including "open", "closed", and "inactivated". Their hypotheses were confirmed in the mid-1970s and 1980s by [[Erwin Neher]] and [[Bert Sakmann]], who developed the technique of [[patch clamp]]ing to examine the conductance states of individual ion channels.<ref name="patch_clamp" group="lower-alpha">{{cite journal | vauthors = Neher E, Sakmann B | title = Single-channel currents recorded from membrane of denervated frog muscle fibres | journal = Nature | volume = 260 | issue = 5554 | pages = 799–802 | date = April 1976 | pmid = 1083489 | doi = 10.1038/260799a0 | author-link1 = Erwin Neher | bibcode = 1976Natur.260..799N | s2cid = 4204985 }}<br />* {{cite journal | vauthors = Hamill OP, Marty A, Neher E, Sakmann B, Sigworth FJ | title = Improved patch-clamp techniques for high-resolution current recording from cells and cell-free membrane patches | journal = Pflügers Archiv | volume = 391 | issue = 2 | pages = 85–100 | date = August 1981 | pmid = 6270629 | doi = 10.1007/BF00656997 | s2cid = 12014433 }}<br />* {{cite journal | vauthors = Neher E, Sakmann B | title = The patch clamp technique | journal = Scientific American | volume = 266 | issue = 3 | pages = 44–51 | date = March 1992 | pmid = 1374932 | doi = 10.1038/scientificamerican0392-44 | author-link1 = Erwin Neher | bibcode = 1992SciAm.266c..44N }}</ref> In the 21st century, researchers are beginning to understand the structural basis for these conductance states and for the selectivity of channels for their species of ion,<ref name="yellen_2002" group="lower-alpha">{{cite journal | vauthors = Yellen G | title = The voltage-gated potassium channels and their relatives | journal = Nature | volume = 419 | issue = 6902 | pages = 35–42 | date = September 2002 | pmid = 12214225 | doi = 10.1038/nature00978 | bibcode = 2002Natur.419...35Y | s2cid = 4420877 }}</ref> through the atomic-resolution [[X-ray crystallography|crystal structures]],<ref name="doyle_1998" group="lower-alpha">{{cite journal | vauthors = Doyle DA, Morais Cabral J, Pfuetzner RA, Kuo A, Gulbis JM, Cohen SL, Chait BT, MacKinnon R | display-authors = 6 | title = The structure of the potassium channel: molecular basis of K+ conduction and selectivity | journal = Science | volume = 280 | issue = 5360 | pages = 69–77 | date = April 1998 | pmid = 9525859 | doi = 10.1126/science.280.5360.69 | bibcode = 1998Sci...280...69D }}<br />* {{cite journal | vauthors = Zhou Y, Morais-Cabral JH, Kaufman A, MacKinnon R | title = Chemistry of ion coordination and hydration revealed by a K+ channel-Fab complex at 2.0 A resolution | journal = Nature | volume = 414 | issue = 6859 | pages = 43–8 | date = November 2001 | pmid = 11689936 | doi = 10.1038/35102009 | bibcode = 2001Natur.414...43Z | s2cid = 205022645 }}<br />* {{cite journal | vauthors = Jiang Y, Lee A, Chen J, Ruta V, Cadene M, Chait BT, MacKinnon R | title = X-ray structure of a voltage-dependent K+ channel | journal = Nature | volume = 423 | issue = 6935 | pages = 33–41 | date = May 2003 | pmid = 12721618 | doi = 10.1038/nature01580 | bibcode = 2003Natur.423...33J | s2cid = 4347957 }}</ref> fluorescence distance measurements<ref name="FRET" group="lower-alpha">{{cite journal | vauthors = Cha A, Snyder GE, Selvin PR, Bezanilla F | title = Atomic scale movement of the voltage-sensing region in a potassium channel measured via spectroscopy | journal = Nature | volume = 402 | issue = 6763 | pages = 809–13 | date = December 1999 | pmid = 10617201 | doi = 10.1038/45552 | bibcode = 1999Natur.402..809C | s2cid = 4353978 }}<br />* {{cite journal | vauthors = Glauner KS, Mannuzzu LM, Gandhi CS, Isacoff EY | title = Spectroscopic mapping of voltage sensor movement in the Shaker potassium channel | journal = Nature | volume = 402 | issue = 6763 | pages = 813–7 | date = December 1999 | pmid = 10617202 | doi = 10.1038/45561 | bibcode = 1999Natur.402..813G | s2cid = 4417476 }}<br />* {{cite journal | vauthors = Bezanilla F | title = The voltage sensor in voltage-dependent ion channels | journal = Physiological Reviews | volume = 80 | issue = 2 | pages = 555–92 | date = April 2000 | pmid = 10747201 | doi = 10.1152/physrev.2000.80.2.555 }}</ref> and [[cryo-electron microscopy]] studies.<ref name="cryoEM" group="lower-alpha">{{cite journal | vauthors = Catterall WA | title = A 3D view of sodium channels | journal = Nature | volume = 409 | issue = 6823 | pages = 988–9, 991 | date = February 2001 | pmid = 11234048 | doi = 10.1038/35059188 | bibcode = 2001Natur.409..988C | s2cid = 4371677 | doi-access = free }}<br />* {{cite journal | vauthors = Sato C, Ueno Y, Asai K, Takahashi K, Sato M, Engel A, Fujiyoshi Y | title = The voltage-sensitive sodium channel is a bell-shaped molecule with several cavities | journal = Nature | volume = 409 | issue = 6823 | pages = 1047–51 | date = February 2001 | pmid = 11234014 | doi = 10.1038/35059098 | bibcode = 2001Natur.409.1047S | s2cid = 4430165 }}</ref>

20世纪是20世纪电生理学的重要时期。1902年和1912年，朱利叶斯 · 伯恩斯坦提出了动作电位是由轴突膜对离子的渗透性改变引起的假说。肯 · 科尔和霍华德 · 柯蒂斯证实了伯恩斯坦的假设，他们发现在动作电位期间膜电导增加。1907年，路易斯 · 拉皮克提出，动作电位产生的阈值被跨越，后来被证明为离子电导动力学系统的乘积。1949年，Alan Hodgkin 和 Bernard Katz 提出了 Bernstein 的假说，他们认为轴突膜对不同的离子可能有不同的通透性; 特别是，他们证明了钠通透性对动作电位的关键作用。他们首次实际记录了神经元膜上的电变化，这些电变化介导了动作电位。这一系列的研究在 Hodgkin，Katz 和 Andrew Huxley 的5篇1952年的论文中达到了顶峰，他们应用电压钳技术来确定轴突膜对钠离子和钾离子的通透性对电压和时间的依赖性，从而能够定量地重建动作电位。< br/> < br/> < br/> < br/> < br/> < Hodgkin 和 Huxley 将其数学模型的性质与离散离子通道相关联，离散离子通道可以存在于几种不同的状态，包括“开放”、“封闭”和“失活”。他们的假设在20世纪70年代中期和80年代得到 Erwin Neher 和 Bert Sakmann 的证实，他们发明了膜片钳技术来检测单个离子通道的电导状态。在21世纪，通过原子分辨率晶体结构，研究人员开始了解这些电导态的结构基础，以及离子种类的通道选择性，荧光距离测量 < br/> < br/> 和冷冻电子显微研究。< br/> *

20世纪是电生理的重要时期。1902年和1912年，Julius Bernstein 提出了动作电位是由轴突膜对离子的渗透性改变引起的假说.<ref name="bernstein_1902_1912" group="lower-alpha" />。Ken Cole 和 Howard Curtis 证实了 Bernstein 的假说，他们发现在动作电位期间膜电导增加.<ref name=":16" group="lower-alpha" /> 。1907年，Louis Lapicque 提出，动作电位产生的阈值被跨越,<ref name=":17" group="lower-alpha" /> w，后来被证明为离子电导动力学系统的乘积。1949年，Alan Hodgkin 和 Bernard Katz 完善了 Bernstein 的假说，他们认为轴突膜对不同的离子可能有不同的通透性; 特别是，他们证明了钠通透性对动作电位的关键作用.<ref name="hodgkin_1949" group="lower-alpha" /> 。他们首次实际记录了神经元膜上的电变化，这些电变化介导了动作电位.<ref name=":0" group="lower-Greek" /> 。这一系列的研究在 Hodgkin，Katz 和 Andrew Huxley 的5篇1952年的论文中达到了顶峰，他们应用电压钳技术来确定轴突膜对钠离子和钾离子的通透性对电压和时间的依赖性，从而能够定量地重建动作电位.<ref name="hodgkin_1952" group="lower-alpha" /> 。Hodgkin 和 Huxley 将其数学模型的性质与离散离子通道相关联，离散离子通道可以存在于几种不同的状态，包括“开放”、“封闭”和“失活”。他们的假设在20世纪70年代中期和80年代得到 Erwin Neher 和 Bert Sakmann 的证实，他们发明了膜片钳技术来检测单个离子通道的电导状态.<ref name="patch_clamp" group="lower-alpha" /> 。在21世纪，通过原子分辨率晶体结构,<ref name="doyle_1998" group="lower-alpha" /> ，研究人员开始了解这些电导态的结构基础，以及离子种类的通道选择性,<ref name="yellen_2002" group="lower-alpha" /> ，荧光距离测量s<ref name="FRET" group="lower-alpha" /> 和冷冻电子显微研究s.<ref name="cryoEM" group="lower-alpha" />。

Julius Bernstein was also the first to introduce the [[Nernst equation]] for [[resting potential]] across the membrane; this was generalized by [[David E. Goldman]] to the eponymous [[Goldman equation]] in 1943.<ref name="goldman_1943" group="lower-alpha" /> The [[sodium–potassium pump]] was identified in 1957<ref group="lower-alpha">{{cite journal | vauthors = Skou JC | title = The influence of some cations on an adenosine triphosphatase from peripheral nerves | journal = Biochimica et Biophysica Acta | volume = 23 | issue = 2 | pages = 394–401 | date = February 1957 | pmid = 13412736 | doi = 10.1016/0006-3002(57)90343-8 }}</ref><ref group="lower-Greek">{{cite press release | url = http://nobelprize.org/nobel_prizes/medicine/laureates/1997/press.html | title = The Nobel Prize in Chemistry 1997 | publisher = The Royal Swedish Academy of Science | year = 1997 | access-date = 2010-02-21 | url-status = live | archive-url = https://web.archive.org/web/20091023003257/http://nobelprize.org/nobel_prizes/medicine/laureates/1997/press.html | archive-date = 23 October 2009 | df = dmy-all }}</ref> and its properties gradually elucidated,<ref name="hodgkin_1955" group="lower-alpha">{{cite journal | vauthors = Hodgkin AL, Keynes RD | title = Active transport of cations in giant axons from Sepia and Loligo | journal = The Journal of Physiology | volume = 128 | issue = 1 | pages = 28–60 | date = April 1955 | pmid = 14368574 | pmc = 1365754 | doi = 10.1113/jphysiol.1955.sp005290 | author-link1 = Alan Lloyd Hodgkin }}</ref><ref name="caldwell_1960" group="lower-alpha">{{cite journal | vauthors = Caldwell PC, Hodgkin AL, Keynes RD, Shaw TL | title = The effects of injecting 'energy-rich' phosphate compounds on the active transport of ions in the giant axons of Loligo | journal = The Journal of Physiology | volume = 152 | issue = 3 | pages = 561–90 | date = July 1960 | pmid = 13806926 | pmc = 1363339 | doi = 10.1113/jphysiol.1960.sp006509 }}</ref><ref name="caldwell_1957" group="lower-alpha">{{cite journal | vauthors = Caldwell PC, Keynes RD | title = The utilization of phosphate bond energy for sodium extrusion from giant axons | journal = The Journal of Physiology | volume = 137 | issue = 1 | pages = 12–3P | date = June 1957 | pmid = 13439598 | doi = 10.1113/jphysiol.1957.sp005830 | s2cid = 222188054 }}</ref> culminating in the determination of its atomic-resolution structure by [[X-ray crystallography]].<ref name="Na_K_pump_structure" group="lower-alpha">{{cite journal | vauthors = Morth JP, Pedersen BP, Toustrup-Jensen MS, Sørensen TL, Petersen J, Andersen JP, Vilsen B, Nissen P | display-authors = 6 | title = Crystal structure of the sodium-potassium pump | journal = Nature | volume = 450 | issue = 7172 | pages = 1043–9 | date = December 2007 | pmid = 18075585 | doi = 10.1038/nature06419 | bibcode = 2007Natur.450.1043M | s2cid = 4344526 }}</ref> The crystal structures of related ionic pumps have also been solved, giving a broader view of how these [[molecular machine]]s work.<ref group="lower-alpha">{{cite journal | vauthors = Lee AG, East JM | title = What the structure of a calcium pump tells us about its mechanism | journal = The Biochemical Journal | volume = 356 | issue = Pt 3 | pages = 665–83 | date = June 2001 | pmid = 11389676 | pmc = 1221895 | doi = 10.1042/0264-6021:3560665 }}</ref>

Julius Bernstein was also the first to introduce the [[Nernst equation]] for [[resting potential]] across the membrane; this was generalized by [[David E. Goldman]] to the eponymous [[Goldman equation]] in 1943.<ref name="goldman_1943" group="lower-alpha" /> The [[sodium–potassium pump]] was identified in 1957<ref group="lower-alpha" name=":18">{{cite journal | vauthors = Skou JC | title = The influence of some cations on an adenosine triphosphatase from peripheral nerves | journal = Biochimica et Biophysica Acta | volume = 23 | issue = 2 | pages = 394–401 | date = February 1957 | pmid = 13412736 | doi = 10.1016/0006-3002(57)90343-8 }}</ref><ref group="lower-Greek" name=":1">{{cite press release | url = http://nobelprize.org/nobel_prizes/medicine/laureates/1997/press.html | title = The Nobel Prize in Chemistry 1997 | publisher = The Royal Swedish Academy of Science | year = 1997 | access-date = 2010-02-21 | url-status = live | archive-url = https://web.archive.org/web/20091023003257/http://nobelprize.org/nobel_prizes/medicine/laureates/1997/press.html | archive-date = 23 October 2009 | df = dmy-all }}</ref> and its properties gradually elucidated,<ref name="hodgkin_1955" group="lower-alpha">{{cite journal | vauthors = Hodgkin AL, Keynes RD | title = Active transport of cations in giant axons from Sepia and Loligo | journal = The Journal of Physiology | volume = 128 | issue = 1 | pages = 28–60 | date = April 1955 | pmid = 14368574 | pmc = 1365754 | doi = 10.1113/jphysiol.1955.sp005290 | author-link1 = Alan Lloyd Hodgkin }}</ref><ref name="caldwell_1960" group="lower-alpha">{{cite journal | vauthors = Caldwell PC, Hodgkin AL, Keynes RD, Shaw TL | title = The effects of injecting 'energy-rich' phosphate compounds on the active transport of ions in the giant axons of Loligo | journal = The Journal of Physiology | volume = 152 | issue = 3 | pages = 561–90 | date = July 1960 | pmid = 13806926 | pmc = 1363339 | doi = 10.1113/jphysiol.1960.sp006509 }}</ref><ref name="caldwell_1957" group="lower-alpha">{{cite journal | vauthors = Caldwell PC, Keynes RD | title = The utilization of phosphate bond energy for sodium extrusion from giant axons | journal = The Journal of Physiology | volume = 137 | issue = 1 | pages = 12–3P | date = June 1957 | pmid = 13439598 | doi = 10.1113/jphysiol.1957.sp005830 | s2cid = 222188054 }}</ref> culminating in the determination of its atomic-resolution structure by [[X-ray crystallography]].<ref name="Na_K_pump_structure" group="lower-alpha">{{cite journal | vauthors = Morth JP, Pedersen BP, Toustrup-Jensen MS, Sørensen TL, Petersen J, Andersen JP, Vilsen B, Nissen P | display-authors = 6 | title = Crystal structure of the sodium-potassium pump | journal = Nature | volume = 450 | issue = 7172 | pages = 1043–9 | date = December 2007 | pmid = 18075585 | doi = 10.1038/nature06419 | bibcode = 2007Natur.450.1043M | s2cid = 4344526 }}</ref> The crystal structures of related ionic pumps have also been solved, giving a broader view of how these [[molecular machine]]s work.<ref group="lower-alpha" name=":19">{{cite journal | vauthors = Lee AG, East JM | title = What the structure of a calcium pump tells us about its mechanism | journal = The Biochemical Journal | volume = 356 | issue = Pt 3 | pages = 665–83 | date = June 2001 | pmid = 11389676 | pmc = 1221895 | doi = 10.1042/0264-6021:3560665 }}</ref>

也是第一个将静息电位的能斯特方程引入到薄膜上的人; David e. Goldman 在1943年将这个方程推广到了以他的名字命名的戈德曼方程。钠钾泵在1957年被鉴定出来，它的性质逐渐被阐明，最终由 X光散射技术测定了它的原子分辨率结构。相关的离子泵的晶体结构也已经被解决，从而为这些分子机器如何工作提供了更广阔的视野。

Julius Bernstein 也是第一个将静息电位的能斯特方程引入到薄膜上的人; David E. Goldman 在1943年将这个方程推广到了以他的名字命名的戈德曼方程.<ref name="goldman_1943" group="lower-alpha" /> 。钠钾泵在1957年被鉴定出来7<ref name=":18" group="lower-alpha" /><ref name=":1" group="lower-Greek" /> ，它的性质逐渐被阐明,<ref name="hodgkin_1955" group="lower-alpha" /><ref name="caldwell_1960" group="lower-alpha" /><ref name="caldwell_1957" group="lower-alpha" /> culm，最终由 X光散射技术测定了它的原子分辨率结构.<ref name="Na_K_pump_structure" group="lower-alpha" /> 。相关的离子泵的晶体结构也已经被解决，从而为这些分子机器如何工作提供了更广阔的视野.<ref name=":19" group="lower-alpha" />。

==Quantitative models==

==Quantitative models==

[[Image:MembraneCircuit.svg|thumb|336px|right|Equivalent electrical circuit for the Hodgkin–Huxley model of the action potential. ''I_m'' and ''V_m'' represent the current through, and the voltage across, a small patch of membrane, respectively. The ''C_m'' represents the capacitance of the membrane patch, whereas the four ''g'''s represent the [[electrical conductance|conductances]] of four types of ions. The two conductances on the left, for potassium (K) and sodium (Na), are shown with arrows to indicate that they can vary with the applied voltage, corresponding to the [[voltage-gated ion channel|voltage-sensitive ion channels]]. The two conductances on the right help determine the [[resting membrane potential]].|链接=Special:FilePath/MembraneCircuit.svg]]

[[Image:MembraneCircuit.svg|thumb|336px|right|Equivalent electrical circuit for the Hodgkin–Huxley model of the action potential. ''I_m'' and ''V_m'' represent the current through, and the voltage across, a small patch of membrane, respectively. The ''C_m'' represents the capacitance of the membrane patch, whereas the four ''g'''s represent the [[electrical conductance|conductances]] of four types of ions. The two conductances on the left, for potassium (K) and sodium (Na), are shown with arrows to indicate that they can vary with the applied voltage, corresponding to the [[voltage-gated ion channel|voltage-sensitive ion channels]]. The two conductances on the right help determine the [[resting membrane potential]].|链接=Special:FilePath/MembraneCircuit.svg]]

Mathematical and computational models are essential for understanding the action potential, and offer predictions that may be tested against experimental data, providing a stringent test of a theory. The most important and accurate of the early neural models is the [[Hodgkin–Huxley model]], which describes the action potential by a coupled set of four [[ordinary differential equation]]s (ODEs).<ref name="hodgkin_1952" group="lower-alpha" /> Although the Hodgkin–Huxley model may be a simplification with few limitations<ref>{{cite journal | vauthors = Baranauskas G, Martina M | title = Sodium currents activate without a Hodgkin-and-Huxley-type delay in central mammalian neurons | journal = The Journal of Neuroscience | volume = 26 | issue = 2 | pages = 671–84 | date = January 2006 | pmid = 16407565 | pmc = 6674426 | doi = 10.1523/jneurosci.2283-05.2006 }}</ref> compared to the realistic nervous membrane as it exists in nature, its complexity has inspired several even-more-simplified models,{{sfn|Hoppensteadt|1986}}<ref group="lower-alpha">*{{cite journal | vauthors = Fitzhugh R | title = Thresholds and plateaus in the Hodgkin-Huxley nerve equations | journal = The Journal of General Physiology | volume = 43 | issue = 5 | pages = 867–96 | date = May 1960 | pmid = 13823315 | pmc = 2195039 | doi = 10.1085/jgp.43.5.867 }}<br />* {{cite journal | vauthors = Kepler TB, Abbott LF, Marder E | title = Reduction of conductance-based neuron models | journal = Biological Cybernetics | volume = 66 | issue = 5 | pages = 381–7 | year = 1992 | pmid = 1562643 | doi = 10.1007/BF00197717 | s2cid = 6789007 }}</ref> such as the [[Morris–Lecar model]]<ref name="morris_1981" group="lower-alpha">{{cite journal | vauthors = Morris C, Lecar H | title = Voltage oscillations in the barnacle giant muscle fiber | journal = Biophysical Journal | volume = 35 | issue = 1 | pages = 193–213 | date = July 1981 | pmid = 7260316 | pmc = 1327511 | doi = 10.1016/S0006-3495(81)84782-0 | bibcode = 1981BpJ....35..193M }}</ref> and the [[FitzHugh–Nagumo model]],<ref name="fitzhugh" group="lower-alpha">{{cite journal | vauthors = Fitzhugh R | title = Impulses and Physiological States in Theoretical Models of Nerve Membrane | journal = Biophysical Journal | volume = 1 | issue = 6 | pages = 445–66 | date = July 1961 | pmid = 19431309 | pmc = 1366333 | doi = 10.1016/S0006-3495(61)86902-6 | bibcode = 1961BpJ.....1..445F }}<br />* {{cite journal | vauthors = Nagumo J, Arimoto S, Yoshizawa S | year = 1962 | title = An active pulse transmission line simulating nerve axon | journal = Proceedings of the IRE | volume = 50 | pages = 2061–2070 | doi = 10.1109/JRPROC.1962.288235 | issue = 10 | s2cid = 51648050 }}</ref> both of which have only two coupled ODEs. The properties of the Hodgkin–Huxley and FitzHugh–Nagumo models and their relatives, such as the Bonhoeffer–Van der Pol model,<ref name="bonhoeffer_vanderPol" group="lower-alpha">{{cite journal | vauthors = Bonhoeffer KF | title = Activation of passive iron as a model for the excitation of nerve | journal = The Journal of General Physiology | volume = 32 | issue = 1 | pages = 69–91 | date = September 1948 | pmid = 18885679 | pmc = 2213747 | doi = 10.1085/jgp.32.1.69 }}<br />* {{cite journal | vauthors = Bonhoeffer KF | year = 1953 | title = Modelle der Nervenerregung | journal = Naturwissenschaften | volume = 40 | pages = 301–311 | doi = 10.1007/BF00632438|bibcode = 1953NW.....40..301B | issue = 11 | s2cid = 19149460 }}<br />* {{cite journal | vauthors = Van der Pol B | year = 1926 | title = On relaxation-oscillations | journal = Philosophical Magazine | volume = 2 | pages = 977–992| author-link = Balthasar van der Pol }}<br />* {{cite journal | year = 1928 | title = The heartbeat considered as a relaxation oscillation, and an electrical model of the heart | journal = Philosophical Magazine | volume = 6 | pages = 763–775| vauthors = Van der Pol B, Van der Mark J| author-link1 = Balthasar van der Pol | doi=10.1080/14786441108564652}}<br />* {{cite journal | year = 1929 | title = The heartbeat considered as a relaxation oscillation, and an electrical model of the heart | journal = Arch. Neerl. Physiol. | volume = 14 | pages = 418–443| vauthors = Van der Pol B, van der Mark J| author-link1 = Balthasar van der Pol }}</ref> have been well-studied within mathematics,<ref name="math_studies">Sato, S; Fukai, H; Nomura, T; Doi, S in {{harvnb|Reeke|Poznanski|Sporns|Rosenberg|2005|loc=''Bifurcation Analysis of the Hodgkin-Huxley Equations'', pp. 459–478.}}<br />* FitzHugh, R in {{harvnb|Schwann|1969|loc=''Mathematical models of axcitation and propagation in nerve'', pp. 12–16.}}<br />* {{harvnb|Guckenheimer|Holmes|1986|pp=12–16}}</ref><ref group="lower-alpha">{{cite journal | vauthors = Evans JW | year = 1972 | title = Nerve axon equations. I. Linear approximations | journal = Indiana Univ. Math. J. | volume = 21 | pages = 877–885 | doi = 10.1512/iumj.1972.21.21071 | issue = 9| doi-access = free }}<br />* {{cite journal | vauthors = Evans JW, Feroe J | year = 1977 | title = Local stability theory of the nerve impulse | journal = Math. Biosci. | volume = 37 | pages = 23–50 | doi = 10.1016/0025-5564(77)90076-1 }}</ref> computation<ref name="computational_studies">Nelson, ME; Rinzel, J in {{harvnb|Bower|Beeman|1995|loc=''The Hodgkin-Huxley Model'', pp. 29–49.}}<br />* Rinzel, J & Ermentrout, GB; in {{harvnb|Koch|Segev|1989|loc=''Analysis of Neural Excitability and Oscillations'', pp. 135–169.}}</ref> and electronics.<ref name="keener_1983" group="lower-alpha">{{cite journal | vauthors = Keener JP | year = 1983 | title = Analogue circuitry for the Van der Pol and FitzHugh-Nagumo equations | journal = IEEE Transactions on Systems, Man and Cybernetics | volume = 13 | issue = 5 | pages = 1010–1014 | doi = 10.1109/TSMC.1983.6313098 | s2cid = 20077648 }}</ref> However the simple models of generator potential and action potential fail to accurately reproduce the near threshold neural spike rate and spike shape, specifically for the [[mechanoreceptors]] like the [[Pacinian corpuscle]].<ref>{{cite journal | vauthors = Biswas A, Manivannan M, Srinivasan MA | title = Vibrotactile sensitivity threshold: nonlinear stochastic mechanotransduction model of the Pacinian Corpuscle | journal = IEEE Transactions on Haptics | volume = 8 | issue = 1 | pages = 102–13 | year = 2015 | pmid = 25398183 | doi = 10.1109/TOH.2014.2369422 | s2cid = 15326972 | url = https://zenodo.org/record/894772 }}</ref> More modern research has focused on larger and more integrated systems; by joining action-potential models with models of other parts of the nervous system (such as dendrites and synapses), researchers can study [[neural computation]]{{sfnm|1a1=McCulloch|1y=1988|1pp=19–39, 46–66, 72–141|2a1=Anderson|2a2=Rosenfeld|2y=1988|2pp=15–41}} and simple [[reflex]]es, such as [[escape reflex]]es and others controlled by [[central pattern generator]]s.<ref name="cpg">Getting, PA in {{harvnb|Koch|Segev|1989|loc=''Reconstruction of Small Neural Networks'', pp. 171–194.}}</ref><ref name="pmid10713861" group="lower-alpha">{{cite journal | vauthors = Hooper SL | title = Central pattern generators | journal = Current Biology | volume = 10 | issue = 5 | pages = R176–R179 | date = March 2000 | pmid = 10713861 | doi = 10.1016/S0960-9822(00)00367-5 | citeseerx = 10.1.1.133.3378 | s2cid = 11388348 }}</ref>

Mathematical and computational models are essential for understanding the action potential, and offer predictions that may be tested against experimental data, providing a stringent test of a theory. The most important and accurate of the early neural models is the [[Hodgkin–Huxley model]], which describes the action potential by a coupled set of four [[ordinary differential equation]]s (ODEs).<ref name="hodgkin_1952" group="lower-alpha" /> Although the Hodgkin–Huxley model may be a simplification with few limitations<ref name=":23">{{cite journal | vauthors = Baranauskas G, Martina M | title = Sodium currents activate without a Hodgkin-and-Huxley-type delay in central mammalian neurons | journal = The Journal of Neuroscience | volume = 26 | issue = 2 | pages = 671–84 | date = January 2006 | pmid = 16407565 | pmc = 6674426 | doi = 10.1523/jneurosci.2283-05.2006 }}</ref> compared to the realistic nervous membrane as it exists in nature, its complexity has inspired several even-more-simplified models,{{sfn|Hoppensteadt|1986}}<ref group="lower-alpha" name=":20">*{{cite journal | vauthors = Fitzhugh R | title = Thresholds and plateaus in the Hodgkin-Huxley nerve equations | journal = The Journal of General Physiology | volume = 43 | issue = 5 | pages = 867–96 | date = May 1960 | pmid = 13823315 | pmc = 2195039 | doi = 10.1085/jgp.43.5.867 }}<br />* {{cite journal | vauthors = Kepler TB, Abbott LF, Marder E | title = Reduction of conductance-based neuron models | journal = Biological Cybernetics | volume = 66 | issue = 5 | pages = 381–7 | year = 1992 | pmid = 1562643 | doi = 10.1007/BF00197717 | s2cid = 6789007 }}</ref> such as the [[Morris–Lecar model]]<ref name="morris_1981" group="lower-alpha">{{cite journal | vauthors = Morris C, Lecar H | title = Voltage oscillations in the barnacle giant muscle fiber | journal = Biophysical Journal | volume = 35 | issue = 1 | pages = 193–213 | date = July 1981 | pmid = 7260316 | pmc = 1327511 | doi = 10.1016/S0006-3495(81)84782-0 | bibcode = 1981BpJ....35..193M }}</ref> and the [[FitzHugh–Nagumo model]],<ref name="fitzhugh" group="lower-alpha">{{cite journal | vauthors = Fitzhugh R | title = Impulses and Physiological States in Theoretical Models of Nerve Membrane | journal = Biophysical Journal | volume = 1 | issue = 6 | pages = 445–66 | date = July 1961 | pmid = 19431309 | pmc = 1366333 | doi = 10.1016/S0006-3495(61)86902-6 | bibcode = 1961BpJ.....1..445F }}<br />* {{cite journal | vauthors = Nagumo J, Arimoto S, Yoshizawa S | year = 1962 | title = An active pulse transmission line simulating nerve axon | journal = Proceedings of the IRE | volume = 50 | pages = 2061–2070 | doi = 10.1109/JRPROC.1962.288235 | issue = 10 | s2cid = 51648050 }}</ref> both of which have only two coupled ODEs. The properties of the Hodgkin–Huxley and FitzHugh–Nagumo models and their relatives, such as the Bonhoeffer–Van der Pol model,<ref name="bonhoeffer_vanderPol" group="lower-alpha">{{cite journal | vauthors = Bonhoeffer KF | title = Activation of passive iron as a model for the excitation of nerve | journal = The Journal of General Physiology | volume = 32 | issue = 1 | pages = 69–91 | date = September 1948 | pmid = 18885679 | pmc = 2213747 | doi = 10.1085/jgp.32.1.69 }}<br />* {{cite journal | vauthors = Bonhoeffer KF | year = 1953 | title = Modelle der Nervenerregung | journal = Naturwissenschaften | volume = 40 | pages = 301–311 | doi = 10.1007/BF00632438|bibcode = 1953NW.....40..301B | issue = 11 | s2cid = 19149460 }}<br />* {{cite journal | vauthors = Van der Pol B | year = 1926 | title = On relaxation-oscillations | journal = Philosophical Magazine | volume = 2 | pages = 977–992| author-link = Balthasar van der Pol }}<br />* {{cite journal | year = 1928 | title = The heartbeat considered as a relaxation oscillation, and an electrical model of the heart | journal = Philosophical Magazine | volume = 6 | pages = 763–775| vauthors = Van der Pol B, Van der Mark J| author-link1 = Balthasar van der Pol | doi=10.1080/14786441108564652}}<br />* {{cite journal | year = 1929 | title = The heartbeat considered as a relaxation oscillation, and an electrical model of the heart | journal = Arch. Neerl. Physiol. | volume = 14 | pages = 418–443| vauthors = Van der Pol B, van der Mark J| author-link1 = Balthasar van der Pol }}</ref> have been well-studied within mathematics,<ref name="math_studies">Sato, S; Fukai, H; Nomura, T; Doi, S in {{harvnb|Reeke|Poznanski|Sporns|Rosenberg|2005|loc=''Bifurcation Analysis of the Hodgkin-Huxley Equations'', pp. 459–478.}}<br />* FitzHugh, R in {{harvnb|Schwann|1969|loc=''Mathematical models of axcitation and propagation in nerve'', pp. 12–16.}}<br />* {{harvnb|Guckenheimer|Holmes|1986|pp=12–16}}</ref><ref group="lower-alpha" name=":21">{{cite journal | vauthors = Evans JW | year = 1972 | title = Nerve axon equations. I. Linear approximations | journal = Indiana Univ. Math. J. | volume = 21 | pages = 877–885 | doi = 10.1512/iumj.1972.21.21071 | issue = 9| doi-access = free }}<br />* {{cite journal | vauthors = Evans JW, Feroe J | year = 1977 | title = Local stability theory of the nerve impulse | journal = Math. Biosci. | volume = 37 | pages = 23–50 | doi = 10.1016/0025-5564(77)90076-1 }}</ref> computation<ref name="computational_studies">Nelson, ME; Rinzel, J in {{harvnb|Bower|Beeman|1995|loc=''The Hodgkin-Huxley Model'', pp. 29–49.}}<br />* Rinzel, J & Ermentrout, GB; in {{harvnb|Koch|Segev|1989|loc=''Analysis of Neural Excitability and Oscillations'', pp. 135–169.}}</ref> and electronics.<ref name="keener_1983" group="lower-alpha">{{cite journal | vauthors = Keener JP | year = 1983 | title = Analogue circuitry for the Van der Pol and FitzHugh-Nagumo equations | journal = IEEE Transactions on Systems, Man and Cybernetics | volume = 13 | issue = 5 | pages = 1010–1014 | doi = 10.1109/TSMC.1983.6313098 | s2cid = 20077648 }}</ref> However the simple models of generator potential and action potential fail to accurately reproduce the near threshold neural spike rate and spike shape, specifically for the [[mechanoreceptors]] like the [[Pacinian corpuscle]].<ref name=":24">{{cite journal | vauthors = Biswas A, Manivannan M, Srinivasan MA | title = Vibrotactile sensitivity threshold: nonlinear stochastic mechanotransduction model of the Pacinian Corpuscle | journal = IEEE Transactions on Haptics | volume = 8 | issue = 1 | pages = 102–13 | year = 2015 | pmid = 25398183 | doi = 10.1109/TOH.2014.2369422 | s2cid = 15326972 | url = https://zenodo.org/record/894772 }}</ref> More modern research has focused on larger and more integrated systems; by joining action-potential models with models of other parts of the nervous system (such as dendrites and synapses), researchers can study [[neural computation]]{{sfnm|1a1=McCulloch|1y=1988|1pp=19–39, 46–66, 72–141|2a1=Anderson|2a2=Rosenfeld|2y=1988|2pp=15–41}} and simple [[reflex]]es, such as [[escape reflex]]es and others controlled by [[central pattern generator]]s.<ref name="cpg">Getting, PA in {{harvnb|Koch|Segev|1989|loc=''Reconstruction of Small Neural Networks'', pp. 171–194.}}</ref><ref name="pmid10713861" group="lower-alpha">{{cite journal | vauthors = Hooper SL | title = Central pattern generators | journal = Current Biology | volume = 10 | issue = 5 | pages = R176–R179 | date = March 2000 | pmid = 10713861 | doi = 10.1016/S0960-9822(00)00367-5 | citeseerx = 10.1.1.133.3378 | s2cid = 11388348 }}</ref>

 

 

数学模型和计算模型对于理解动作电位是必不可少的，它们提供的预测可以通过实验数据进行检验，从而为理论提供严格的检验。早期神经模型中最重要和最准确的是 Hodgkin-Huxley 模型，它通过一组四个常微分方程(ODEs)来描述动作电位.<ref name="hodgkin_1952" group="lower-alpha" /> 。虽然 Hodgkin-Huxley 模型可能是一个简化的模型,{{sfn|Hoppensteadt|1986}}<ref name=":20" group="lower-alpha" /> s，但与实际存在的神经膜相比，它的局限性很小s<ref name=":23" />，其复杂性激发了几个更简化的模型，例如 Morris-Lecar 模型[[Morris–Lecar model|l]]<ref name="morris_1981" group="lower-alpha" /> a和 FitzHugh-Nagumo 模型,<ref name="fitzhugh" group="lower-alpha" />，< br/> * 这两个模型都只有两个耦合的常微分方程。Hodgkin-Huxley 模型和 FitzHugh-Nagumo 模型以及它们的近亲，如 Bonhoeffer-Van der Pol 模型l,<ref name="bonhoeffer_vanderPol" group="lower-alpha" />， 已经在数学中得到了很好的研究,<ref name="math_studies" /><ref name=":21" group="lower-alpha" /> c，computationn<ref name="computational_studies" /> Nelson，ME; Rinzel，j in </> * Rinzel，j & ertrout，GB; in electronics.<ref name="keener_1983" group="lower-alpha" /> ;。然而，简单的生成电位和动作电位模型并不能准确地再现近阈值神经元刺激速率和刺激形态，特别是对于机械性受体如太平洋小体.<ref name=":24" /> 。更多的现代研究侧重于更大、更完整的系统; 通过将动作电位模型与神经系统其他部分的模型(如树突和突触)结合起来，研究人员可以研究神经计算和简单反射，如逃逸反射和其他由中枢模式发生器控制的反射.<ref name="cpg" /><ref name="pmid10713861" group="lower-alpha" />。

数学模型和计算模型对于理解动作电位是必不可少的，它们提供的预测可以通过实验数据进行检验，从而为理论提供严格的检验。早期神经模型中最重要和最准确的是 Hodgkin-Huxley 模型，它通过一组四个常微分方程(ODEs)来描述动作电位。虽然 Hodgkin-Huxley 模型可能是一个简化的模型，但与实际存在的神经膜相比，它的局限性很小，其复杂性激发了几个更简化的模型，* < br/> * ，例如 Morris-Lecar 模型和 FitzHugh-Nagumo 模型，< br/> * 这两个模型都只有两个耦合的常微分方程。Hodgkin-Huxley 模型和 FitzHugh-Nagumo 模型以及它们的近亲，如 Bonhoeffer-Van der Pol 模型，< br/> * < br/> * < br/> * < br/> * < br/> * < br/> * < br/> * < br/> * 已经在数学中得到了很好的研究，Sato，s; Fukai，h; Nomura，t; Doi，s in < br/> * FitzHugh，r in < br/> * < br/> * computationNelson，ME; Rinzel，j in </> * Rinzel，j & ertrout，GB; in electronics;。然而，简单的生成电位和动作电位模型并不能准确地再现近阈值神经元刺激速率和刺激形态，特别是对于机械性受体如太平洋小体。更多的现代研究侧重于更大、更完整的系统; 通过将动作电位模型与神经系统其他部分的模型(如树突和突触)结合起来，研究人员可以研究神经计算和简单反射，如逃逸反射和其他由中枢模式发生器控制的反射。进入，PA 进入

 

== See also ==

{{col div|colwidth=40em}}

*[[Single-unit recording]]

 

 

 

 

==Notes==

==Notes==

* {{cite book | veditors = Worden FG, Swazey JP, Adelman G | year = 1975 | title = The Neurosciences, Paths of Discovery | publisher = The MIT Press | location = Cambridge, Massachusetts | isbn = 978-0-262-23072-8 | lccn = 75016379 | oclc = 1500233 | url = https://archive.org/details/TheNeurosc_00_Word }}

* {{cite book | veditors = Worden FG, Swazey JP, Adelman G | year = 1975 | title = The Neurosciences, Paths of Discovery | publisher = The MIT Press | location = Cambridge, Massachusetts | isbn = 978-0-262-23072-8 | lccn = 75016379 | oclc = 1500233 | url = https://archive.org/details/TheNeurosc_00_Word }}

{{Refend}}

{{Refend}}

*  

*  

*  

*  

*  

*  

*  

*  

===Books===

===Books===

* {{cite book | vauthors = Nelson DL, Cox MM | year = 2008 | title = Lehninger Principles of Biochemistry | edition = 5th | publisher = W. H. Freeman | location = New York | isbn = 978-0-7167-7108-1 | url = https://archive.org/details/lehningerprincip00lehn_1 }}

* {{cite book | vauthors = Nelson DL, Cox MM | year = 2008 | title = Lehninger Principles of Biochemistry | edition = 5th | publisher = W. H. Freeman | location = New York | isbn = 978-0-7167-7108-1 | url = https://archive.org/details/lehningerprincip00lehn_1 }}

{{Refend}}

{{Refend}}

 

= External links =

 

 

 

 

== External links ==

{{Spoken Wikipedia|Action_potential.ogg|date=2005-06-22}}

{{Spoken Wikipedia|Action_potential.ogg|date=2005-06-22}}

*[https://web.archive.org/web/20070615135508/http://www.blackwellpublishing.com/matthews/actionp.html Action potential propagation in myelinated and unmyelinated axons] at [[Blackwell Publishing]]

*[https://web.archive.org/web/20070615135508/http://www.blackwellpublishing.com/matthews/actionp.html Action potential propagation in myelinated and unmyelinated axons] at [[Blackwell Publishing]]

*[http://thevirtualheart.org/CAPindex.html Generation of AP in cardiac cells] and [http://thevirtualheart.org/java/neuron/apneuron.html generation of AP in neuron cells]

*[http://thevirtualheart.org/CAPindex.html Generation of AP in cardiac cells] and [http://thevirtualheart.org/java/neuron/apneuron.html generation of AP in neuron cells]

*[https://web.archive.org/web/20080414190744/http://bcs.whfreeman.com/thelifewire/content/chp44/4402001.html Resting membrane potential] from ''Life: The Science of Biology'', by WK Purves, D Sadava, GH Orians, and HC Heller, 8th edition, New York: WH Freeman, {{ISBN|978-0-7167-7671-0}}.

*[https://web.archive.org/web/20080414190744/http://bcs.whfreeman.com/thelifewire/content/chp44/4402001.html Resting membrane potential] from ''Life: The Science of Biology'', by WK Purves, D Sadava, GH Orians, and HC Heller, 8th edition, New York: WH Freeman,

*[https://web.archive.org/web/20100808191814/http://www.nernstgoldman.physiology.arizona.edu/ Ionic motion and the Goldman voltage for arbitrary ionic concentrations] at The [[University of Arizona]]

*[https://web.archive.org/web/20100808191814/http://www.nernstgoldman.physiology.arizona.edu/ Ionic motion and the Goldman voltage for arbitrary ionic concentrations] at The [[University of Arizona]]

*[https://web.archive.org/web/20081216233745/http://www.brainu.org/files/movies/action_potential_cartoon.swf A cartoon illustrating the action potential]

*[https://web.archive.org/web/20081216233745/http://www.brainu.org/files/movies/action_potential_cartoon.swf A cartoon illustrating the action potential]

* Introduction to the Action Potential, Neuroscience Online (electronic neuroscience textbook by UT Houston Medical School)

* Introduction to the Action Potential, Neuroscience Online (electronic neuroscience textbook by UT Houston Medical School)

* Khan Academy: Electrotonic and action potential

* Khan Academy: Electrotonic and action potential

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类别: 电容器类别: 神经编码类别: 电生理学类别: 电化学类别: 计算神经科学类别: 细胞神经科学类别: 细胞过程类别: 膜生物学类别: 植物认知类别: 动作电位

类别: 电容器类别: 神经编码类别: 电生理学类别: 电化学类别: 计算神经科学类别: 细胞神经科学类别: 细胞过程类别: 膜生物学类别: 植物认知类别: 动作电位

<small>This page was moved from [[wikipedia:en:Action potential]]. Its edit history can be viewed at [[动作电位/edithistory]]</small>

 

<small>This page was moved from [[wikipedia:en:Action potential]]. Its edit history can be viewed at [[动作电位/edithistory]]</small></noinclude>

{{DEFAULTSORT:Action Potential}}

{{DEFAULTSORT:Action Potential}}