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第3行： − + − 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.+ − 生理学上，当特定细胞位置的膜电位快速上升和下降时，就会产生动作电位（AP）<ref name=":3" /> ：这种去极化会导致相邻位置同样地去极化。动作电位发生在几种类型的动物细胞，称为可兴奋细胞，包括神经元、肌肉细胞、内分泌细胞和一些植物细胞。+ − 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<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]].+ − 动作电位是由嵌入细胞质膜的特殊类型的电压门控离子通道产生的<ref name="pmid17515599" group="lower-alpha" />。这些通道在膜电位处于细胞的（负值）静息电位附近时关闭，而在膜电位增加到精确定义的阈值电压时迅速打开，从而使膜电位去极化<ref name="pmid17515599" group="lower-alpha" />。通道在开放时，允许钠离子内流，改变电化学梯度，进而使膜电位进一步升高到零。这就导致更多的通道打开，产生更大的跨膜电流，等等。这个过程爆发性地发生，直到所有可用的离子通道都打开，从而导致膜电位的大幅上升。钠离子的快速内流导致细胞质膜极性反转，随后离子通道迅速失活。随着钠离子通道的关闭，钠离子不再能进入神经元，然后它们通过主动运输的方式转运到质膜外。然后，钾离子通道被激活，产生一个外向的钾离子电流，使电化梯度回到静息状态。动作电位发生后，有一短暂的负移，称为后超极化（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 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> − − 在动物细胞，有两种基本类型的动作电位。一种是由电压门控钠通道产生，另一种是由电压门控钙通道产生。钠脉冲通常持续不到一毫秒，但钙脉冲可持续100毫秒或更长时间。在某些类型的神经元，缓慢的钙脉冲为钠脉冲的长时间脉冲提供驱动力。另一方面，在心肌细胞，一个初始的快速钠脉冲提供一个“引子”来激发钙脉冲的快速发放，从而产生肌肉收缩<ref name=":4" />。 − − ==Overview 概述== − 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。.<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. − − 细胞的电特性是由细胞周围的膜的结构决定的。细胞膜由脂双分子层组成，其中嵌入更大的蛋白质分子。这种脂双分子层对带电离子的运动产生很强的阻力，因此它起到了绝缘体的作用。相比之下，膜内嵌的大蛋白质提供离子的跨膜通道。动作电位是由通道蛋白驱动的，通道蛋白的结构随着细胞内外电压差而在闭合和开放状态之间切换。这些电压敏感蛋白被称为电压门控离子通道。 − − ===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]] − 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。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.+ − 每一块可兴奋的细胞膜都有两个重要的膜电位：静息电位，即没有干扰时细胞维持的膜电位值，和更高的值称为阈值电位。在典型神经元的轴丘，静息电位电位约为 -70毫伏，阈值电位约为 -55mV。神经元的突触输入导致膜去极化或超极化; 也就是说，它们导致膜电位的升高或降低。当足够的去极化积累使膜电位达到阈值时，动作电位就被触发。当一个动作电位被触发时，膜电位突然上升，然后同样突然下降，通常下降到静息电位以下，保持一段时间。动作电位的形状是固定不变的，这意味着在一个给定的细胞中，所有动作电位的升降幅度和时间过程大致相同。(本文后面将讨论例外情况)。在大多数神经元中，整个过程发生在千分之一秒左右。许多类型的神经元不断地以每秒10-100的速度发放动作电位。然而，有些类型的细胞更安静，可能持续几分钟或更长时间而不发出任何动作电位。+ + − + − + − 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. − #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. − 动作电位产生于细胞膜上特殊类型的电压门控离子通道.<ref name=":7" /> 。电压门控离子通道是一种跨膜蛋白，有3个关键属性：+ − + − + + − Thus, a voltage-gated ion channel tends to be open for some values of the membrane potential, and closed for others. In most cases, however, the relationship between membrane potential and channel state is probabilistic and involves a time delay. Ion channels switch between conformations at unpredictable times: The membrane potential determines the rate of transitions and the probability per unit time of each type of transition.+ − − 因此，电压门控离子通道对膜电位的某些数值倾向于开放，而对其他值倾向于关闭。然而，在大多数情况下，膜电位和离子通道状态之间是概率关系，并且包含时间延迟。离子通道在不可预知的时间里在不同构象之间切换: 膜电位决定状态切换速率和单位时间每种状态切换类型的概率。 − Voltage-gated ion channels are capable of producing action potentials because they can give rise to [[positive feedback]] loops: The membrane potential controls the state of the ion channels, but the state of the ion channels controls the membrane potential. Thus, in some situations, a rise in the membrane potential can cause ion channels to open, thereby causing a further rise in the membrane potential. An action potential occurs when this positive feedback cycle ([[Hodgkin cycle]]) proceeds explosively. The time and amplitude trajectory of the action potential are determined by the biophysical properties of the voltage-gated ion channels that produce it. Several types of channels capable of producing the positive feedback necessary to generate an action potential do exist. Voltage-gated sodium channels are responsible for the fast action potentials involved in nerve conduction. Slower action potentials in muscle cells and some types of neurons are generated by voltage-gated calcium channels. Each of these types comes in multiple variants, with different voltage sensitivity and different temporal dynamics.+ − − thumb|300px|left|Action potential propagation along an axon − 电压门控离子通道能够产生动作电位，因为它们能够产生正反馈回路: 膜电位控制离子通道的状态，而离子通道的状态控制膜电位。因此，在某些情况下，膜电位的上升会导致离子通道打开，从而导致膜电位的进一步上升。当这种正反馈循环(霍奇金循环)爆发性地进行时，就会产生动作电位。电压门控离子通道的生物物理特性决定了动作电位的时间和振幅轨迹。确实存在几种能够产生产生动作电位所必需的正反馈的通道。电压门控性钠通道负责神经传导的快速动作电位。肌细胞和某些类型的神经元的慢动作电位是由电压门控钙通道产生的。每种类型都有多种变体，具有不同的电压灵敏度和不同的时间动力学。+ − 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''<sub>V</sub> channels. (The "V" stands for "voltage".) An ''Na''<sub>V</sub> 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''<sub>V</sub> 通道(“ v”代表“电压”)。''Na''<sub>V</sub> 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''<sub>V</sub> 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''<sub>V</sub> 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<sup>+</sup>) ion. b) Potassium (K<sup>+</sup>) 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<sup>+</sup> and K<sup>+</sup> 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]]+ − {{Anchor|Firing rate|Neural firing rate}}<!-- This anchor is for the bolded terms at the end of this paragraph; if that sentence is moved, this anchor should be moved along with that sentence to the same location in this article.+ − --> − 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 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 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.+ − 在动作电位过程中，电压门控通道的开放所产生的电流通常明显大于最初的刺激电流。因此，动作电位的幅度、持续时间和形状在很大程度上取决于可兴奋膜的性质，而不是刺激的幅度或持续时间。动作电位的这种全或无的特性使它有别于受体电位、电紧张电位、阈下膜电位振荡和突触电位等随刺激强度变化的级量电位。受到电压门控通道的类型、漏电通道、通道分布、离子浓度、膜电容、温度等因素的决定，许多细胞类型和细胞分区中存在多种动作电位类型。+ − 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。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]]. − − 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 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 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" /> − − 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 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.<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" /> 。 − + 第117行：
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无编辑摘要
{{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<sup>+</sup>) and potassium- (K<sup>+</sup>) gated [[Voltage-gated ion channel|ion channels]] open and close as the membrane reaches its [[threshold potential]]. Na<sup>+</sup> channels open at the beginning of the action potential, and Na<sup>+</sup> moves into the axon, causing [[depolarization]]. [[Repolarization]] occurs when the K<sup>+</sup> channels open and K<sup>+</sup> 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<sup>+</sup>) and potassium- (K<sup>+</sup>) gated [[Voltage-gated ion channel|ion channels]] open and close as the membrane reaches its [[threshold potential]]. Na<sup>+</sup> channels open at the beginning of the action potential, and Na<sup>+</sup> moves into the axon, causing [[depolarization]]. [[Repolarization]] occurs when the K<sup>+</sup> channels open and K<sup>+</sup> 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.
当动作电位（神经冲动）沿着轴突行进时，轴突膜上的极性发生变化 。响应来自另一个神经元的信号，钠（Na +）和钾（K +）门控离子通道随着膜达到其阈值电位而打开和关闭。Na+通道在动作电位开始时打开，Na+进入轴突，导致去极化。 当K+通道打开并且K+移出轴突时，就会发生重极化，从而在电池外部和内部之间产生极性变化。脉冲仅在一个方向上沿着轴突行进，到达轴突末端，在那里它向其他神经元发出信号。|链接=Special:FilePath/Action_Potential.gif]]
生理学上，动作电位（action potential, AP）就是特定细胞位置的膜电位迅速上升又迅速下降的过程<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> ：这种去极化会导致相邻位置同样地去极化。动作电位可在神经元、肌肉细胞、内分泌细胞等类型的称为可兴奋细胞（excitable cells）的动物细胞以及某些植物细胞中发生。
在神经元中，动作电位在细胞与细胞之间的通讯中起着中心作用，它可以以跳跃式传导（saltatory conduction ）方式，协助神经信号沿着轴突向位于轴突末端的突触结传播； 然后信号通过突触传递到其他神经元、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，动作电位是引起肌肉收缩的一系列事件的第一步。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">{{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>。神经元的动作电位也被称为“神经冲动（neural impulse）”或“脉冲（spike）”，神经元产生的动作电位的时间序列被称为“动作电位序列（spike train）”。神经元发出动作电位或神经冲动，也常说神经在“发放（fire）”。
动作电位是由细胞质膜内嵌的特殊类型的电压门控离子通道（voltage-gated ion channel）产生的<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>。这些通道在膜电位处于细胞的静息电位（一个负数数值）附近时关闭，而在膜电位增加到精确定义的阈电位（threshold voltage）时迅速打开，从而使膜电位去极化<ref name="pmid17515599" group="lower-alpha" />。开放状态的通道让钠离子内流，改变电化学梯度，进而使膜电位趋升于零。这便导致更多的通道打开，产生更大的跨膜电流……这个过程爆发性地发生，直到所有可用的离子通道都打开，从而导致膜电位的大幅上升。钠离子的快速内流导致细胞质膜极性反转，随后离子通道迅速失活。随着钠离子通道的关闭，钠离子不再能进入神经元，然后以主动运输的方式被转运到质膜外。随后，钾离子通道被激活，产生一个外向的钾离子电流，使电化学梯度回到静息状态。动作电位发生后，会有短暂的负移，称为后超极化（afterhyperpolarization）。
动物细胞中存在两种基本类型的动作电位。一种是电压门控钠通道产生的，另一种是电压门控钙通道产生的。钠脉冲通常持续不到一毫秒，而钙脉冲可持续 100 毫秒甚至更长时间。在某些类型的神经元，持续稍久的钙脉冲为钠脉冲的长时间迸发提供驱动力。另一方面，在心肌细胞，初始的快速钠脉冲像“点火器”一样，迅速引发钙脉冲，从而产生肌肉收缩<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>。
==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]]
动物、植物和真菌的细胞膜几乎都在细胞外部和内部维持一个电压差，称为膜电位（membrane potential）。动物细胞的跨膜电压一般是 -70 mV。这意味着细胞内部相对于外部存在一个负电压。在大多数类型的细胞中，膜电位通常相当稳定。而某些类型的细胞具有电活性，即它们的电压随着时间而波动。在某些类型的有电活性的细胞，包括神经元和肌肉细胞中，电压波动的通常形式为迅速上升而后迅速下降。这些升降的循环即为动作电位。在某些类型的神经元中，整个升降循环在千分之几秒内发生。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">{{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>。
细胞的电特性是由细胞周围的质膜的结构决定的。细胞膜由内嵌更大的蛋白质分子的脂双分子层组成。这种脂双分子层对带电离子的运动产生很强的阻力，因此产生绝缘作用。而质膜内嵌的大蛋白质可作离子的跨膜通道。驱动动作电位的通道蛋白随细胞内外电压差的变化，而在闭合和开放状态的构象之间转换。这些电压敏感蛋白被称为电压门控离子通道。
===典型的神经元过程===
[[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.
==Biophysical basis 生物物理基础==
典型动作电位的近似图显示了动作电位通过细胞膜上的一个点时的各个阶段。膜电位在时间零点开始时约为−70 mV。在时间 = 1 ms 处施加激励，这会将膜电位提高到 −55 mV（阈值电位）以上。施加刺激后，膜电位在时间= 2 ms时迅速上升到+40 mV的峰值电位。同样快速，电位在时间 = 3 ms 时下降并过冲至 −90 mV，最后在时间 = 5 ms 时重新建立 −70 mV 的静息电位。|链接=Special:FilePath/Action_potential.svg]]
{{more citations needed section|date=February 2014}}
动物身体组织中的细胞都是电极化的——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中产生的。神经元细胞膜上的离子通道在不同的细胞部位而类型不同，因而树突、轴突和胞体具有不同的电特性。因此，神经元质膜仅在某些部位是可兴奋的（能够产生动作电位）。近年的研究表明，神经元最易兴奋的部位是轴丘（轴突出离胞体的部位）后的部位，称为轴突始段（axonal initial segment），但在大多数情况下轴突和胞体也是可兴奋的<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>。
可兴奋的细胞膜片都有两个重要的膜电位：未受干扰时细胞维持的静息电位（resting potential），和更高值的阈电位。典型神经元的轴丘的静息电位约为 -70 mV，阈值电位约为 -55 mV。神经元的突触输入导致膜去极化或超极化，即它们使膜电位升高或降低。当去极化累积到足以使膜电位达到阈电位时，就会触发动作电位。动作电位被触发时，膜电位猝然上升，随后同样猝然下降，且常降到静息电位以下一段时间。动作电位的波形是固定不变的，这意味着在给定的细胞中，所有动作电位的升降幅度和时间过程大致相同（本文后面将讨论例外情况）。在大多数神经元中，整个过程发生在千分之一秒左右。很多类型的神经元不断地以每秒 10-100 次的速度发放动作电位。而有些类型更安静的细胞，可能持续几分钟或更长时间而不发生任何动作电位。
==生物物理基础==
#它能够呈现多个构象。
动作电位因细胞膜上特殊类型的电压门控离子通道产生<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> 。电压门控离子通道是一种跨膜蛋白，有三关键性质：
#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。
#它能够呈现多种构象。
#至少一种构象能在膜上形成通道，以渗透特定种类的离子。
#构象之间的转换受到膜电位的影响。
#构象之间的转换受到膜电位的影响。
因此，电压门控离子通道在膜电位处于某些水平时倾向于打开，在其他水平时倾向于关闭。然而，膜电位和离子通道的状态之间在大多数情况下是一种概率关系，并且存在时间延迟。离子通道在不可预测的时间在不同构象之间切换：膜电位决定状态切换速率和单位时间每种切换类型的概率。
[[File:Blausen 0011 ActionPotential Nerve.png|thumb|300px|left|Action potential propagation along an axon|链接=Special:FilePath/Blausen_0011_ActionPotential_Nerve.png]]
[[File:Blausen 0011 ActionPotential Nerve.png|thumb|300px|left|Action potential propagation along an axon|链接=Special:FilePath/Blausen_0011_ActionPotential_Nerve.png]]
电压门控离子通道能够产生动作电位，是因为它们能够产生正反馈回路：膜电位控制离子通道的状态，而离子通道的状态控制膜电位。因此，在某些情况下，膜电位的上升会导致离子通道打开，又导致膜电位的进一步上升。当这种正反馈循环（Hodgkin 循环）爆发性地进行时，就会产生动作电位。电压门控离子通道的生物物理特性决定了动作电位的时间和幅度轨迹。存在几种能产生动作电位所必需的正反馈回路的离子通道。电压门控性钠通道负责神经传导的快速动作电位。肌细胞和某些类型的神经元的稍慢的动作电位是由电压门控钙通道产生的。每种类型都有多种变体，具有不同的电压灵敏度和不同的时间动力学。
研究最多的电压依赖型离子通道是快速神经传导中的钠通道。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关于动作电位的生物物理研究中首先描述的，但更方便地被称为 ''Na''<sub>V</sub> 通道（“ v”代表“电压”）。''Na''<sub>V</sub> 通道有三种可能的状态，即失活（''deactivated''）、激活（''activated''）和灭活（''inactivated''）。这些通道处于激活状态时，允许钠离子通过。当膜电位低时，通道大部分时间处于失活（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。通道一旦被激活，最终会转换到灭火（关闭）状态，并倾向在一段时间内保持灭活状态；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失活→激活→灭活→失活的循环过程。然而这只是群体平均行为——理论上单个通道可在任何时刻发生任何转换。然而，通道从灭活状态直接转换到激活状态的概率极低：处于灭活状态的通道是不应的，直到它回到灭活状态。
这些的结果是，''Na''<sub>V</sub> 通道的动力学决定于状态转换矩阵，其中转换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中起着重要作用，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 为决定离子通道状态的参数建立了一组微分方程，称为 Hodgkin-Huxley 方程（Hodgkin-Huxley equations）。这些方程在后续的研究被修正了很多，但构成很多动作电位生物物理学的理论研究的起点。
[[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<sup>+</sup>) ion. b) Potassium (K<sup>+</sup>) 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<sup>+</sup> and K<sup>+</sup> 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.
动作电位中的离子运动。
图注：a）钠离子（Na<sup>+</sup>），b）钾离子（K<sup>+</sup>），c） 钠通道，d）钾通道，e）钠钾泵。
在动作电位发生的过程中，神经元质膜的通透性发生变化。在'''静息状态'''（1）下，钠离子和钾离子通过膜的能力有限，神经元内部具有净负电荷。一旦触发动作电位，神经元的'''去极化'''（2）激活钠通道，允许钠离子通过细胞膜进入细胞，导致神经元相对于细胞外液的净正电荷。达到动作电位峰值后，神经元开始'''复极化'''（3），其中钠通道关闭，钾通道打开，允许钾离子穿过膜进入细胞外液，使膜电位恢复为负值。最后，有一个'''不应期'''（4），在此期间，电压依赖性离子通道失活，而Na <sup>+</sup>和K <sup>+</sup>离子返回到其在膜上的静息状态分布（1），并且神经元准备重复该过程以获得下一个动作电位。|链接=Special:FilePath/Membrane_Permeability_of_a_Neuron_During_an_Action_Potential.svg]]
随着膜电位的增加，钠离子通道打开，允许钠离子进入细胞。随后钾离子通道打开，允许钾离子流出细胞。钠离子内流增加了细胞中带正电荷的阳离子的浓度，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。膜电位比静息电位高一点时，钾电流超过钠电流，而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关键阈值，通常高于静息值 15 mV ，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。
在动作电位过程中，电压门控通道的开放所产生的电流通常明显大于起初的刺激电流。因此，动作电位的幅度、持续时间和波形在很大程度上取决于可兴奋膜的性质，而不是刺激的幅度或持续时间。动作电位的这种全或无的特性使它有别于受体电位（receptor potentials）、电紧张电位（electrotonic potentials）、阈下膜电位振荡（subthreshold membrane potential oscillations）和突触电位（synaptic potentials）等随刺激强度变化的级量电位。取决于电压门控通道的类型、漏电通道、通道分布、离子浓度、膜电容、温度等因素，许多细胞类型和细胞分区中存在多种动作电位类型。
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，钾离子流出，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。
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">[[Knut Schmidt-Nielsen|Schmidt-Nielsen]], p. 484.</ref>。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。在郎飞节，即规律性间隔的无髓鞘膜片，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，是在信号传播速度和轴突直径之间的折衷。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">{{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>。这些都被认为脉冲时序依赖的突触可塑性（STDP, Spike-timing-dependent_plasticity）中起着重要作用。
在 Hodgkin-Huxley 膜电容模型中，动作电位的传输速度没有定义，而是假设附近区域受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，对熵变和时序的测量中的矛盾，对电容模型是独立工作的产生质疑。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">{{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>。
=== 动作电位的电性质的成熟 ===
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。随着细胞的生长，膜上添加了更多的通道，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，膜电位也会发生更短时间的变化。雪貂外侧膝状核的神经元在 P0 时比在 P30 时有更长的时间常数和更大的电压偏转<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> 。动作电位持续时间减少的一个后果是，可以保持高频刺激的反应信号的保真度。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" /> 。
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（Xenopus）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">{{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> 。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 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>
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.<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" />。
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，通常发生的钠和钾电流密度增加就会被阻止或延迟 <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" />
==Neurotransmission神经传递==
==Neurotransmission神经传递==
===Anatomy of a neuron 神经元解剖===
===Anatomy of a neuron 神经元解剖===
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.
几种类型的细胞支持动作电位，例如植物细胞、肌肉细胞和心脏的特化细胞(在这些细胞中发生心脏动作电位)。然而，最主要的兴奋细胞是神经元，这也有最简单的动作电位机制。
几种类型的细胞支持动作电位，例如植物细胞、肌肉细胞和心脏的特化细胞(在这些细胞中发生心脏动作电位)。然而，最主要的兴奋细胞是神经元，这也有最简单的动作电位机制。
Neurons are electrically excitable cells composed, in general, of one or more dendrites, a single [[soma (biology)|soma]], a single axon and one or more [[axon terminal]]s. Dendrites are cellular projections whose primary function is to receive synaptic signals. Their protrusions, known as [[dendritic spine]]s, are designed to capture the neurotransmitters released by the presynaptic neuron. They have a high concentration of [[ligand-gated ion channel]]s. These spines have a thin neck connecting a bulbous protrusion to the dendrite. This ensures that changes occurring inside the spine are less likely to affect the neighboring spines. The dendritic spine can, with rare exception (see [[Long-term potentiation#Properties|LTP]]), act as an independent unit. The dendrites extend from the soma, which houses the [[Cell nucleus|nucleus]], and many of the "normal" [[eukaryote|eukaryotic]] organelles. Unlike the spines, the surface of the soma is populated by voltage activated ion channels. These channels help transmit the signals generated by the dendrites. Emerging out from the soma is the [[axon hillock]]. This region is characterized by having a very high concentration of voltage-activated sodium channels. In general, it is considered to be the spike initiation zone for action potentials,{{sfn|Bullock|Orkand|Grinnell|1977|p=11}} i.e. the [[trigger zone]]. Multiple signals generated at the spines, and transmitted by the soma all converge here. Immediately after the axon hillock is the axon. This is a thin tubular protrusion traveling away from the soma. The axon is insulated by a [[myelin]] sheath. Myelin is composed of either [[Schwann cells]] (in the peripheral nervous system) or [[oligodendrocytes]] (in the central nervous system), both of which are types of [[glial cells]]. Although glial cells are not involved with the transmission of electrical signals, they communicate and provide important biochemical support to neurons.{{sfn|Silverthorn|2010|p=253}} To be specific, myelin wraps multiple times around the axonal segment, forming a thick fatty layer that prevents ions from entering or escaping the axon. This insulation prevents significant signal decay as well as ensuring faster signal speed. This insulation, however, has the restriction that no channels can be present on the surface of the axon. There are, therefore, regularly spaced patches of membrane, which have no insulation. These [[nodes of Ranvier]] can be considered to be "mini axon hillocks", as their purpose is to boost the signal in order to prevent significant signal decay. At the furthest end, the axon loses its insulation and begins to branch into several [[axon terminal]]s. These presynaptic terminals, or synaptic boutons, are a specialized area within the axon of the presynaptic cell that contains [[neurotransmitters]] enclosed in small membrane-bound spheres called [[synaptic vesicle]]s.
Neurons are electrically excitable cells composed, in general, of one or more dendrites, a single [[soma (biology)|soma]], a single axon and one or more [[axon terminal]]s. Dendrites are cellular projections whose primary function is to receive synaptic signals. Their protrusions, known as [[dendritic spine]]s, are designed to capture the neurotransmitters released by the presynaptic neuron. They have a high concentration of [[ligand-gated ion channel]]s. These spines have a thin neck connecting a bulbous protrusion to the dendrite. This ensures that changes occurring inside the spine are less likely to affect the neighboring spines. The dendritic spine can, with rare exception (see [[Long-term potentiation#Properties|LTP]]), act as an independent unit. The dendrites extend from the soma, which houses the [[Cell nucleus|nucleus]], and many of the "normal" [[eukaryote|eukaryotic]] organelles. Unlike the spines, the surface of the soma is populated by voltage activated ion channels. These channels help transmit the signals generated by the dendrites. Emerging out from the soma is the [[axon hillock]]. This region is characterized by having a very high concentration of voltage-activated sodium channels. In general, it is considered to be the spike initiation zone for action potentials, i.e. the [[trigger zone]]. Multiple signals generated at the spines, and transmitted by the soma all converge here. Immediately after the axon hillock is the axon. This is a thin tubular protrusion traveling away from the soma. The axon is insulated by a [[myelin]] sheath. Myelin is composed of either [[Schwann cells]] (in the peripheral nervous system) or [[oligodendrocytes]] (in the central nervous system), both of which are types of [[glial cells]]. Although glial cells are not involved with the transmission of electrical signals, they communicate and provide important biochemical support to neurons. To be specific, myelin wraps multiple times around the axonal segment, forming a thick fatty layer that prevents ions from entering or escaping the axon. This insulation prevents significant signal decay as well as ensuring faster signal speed. This insulation, however, has the restriction that no channels can be present on the surface of the axon. There are, therefore, regularly spaced patches of membrane, which have no insulation. These [[nodes of Ranvier]] can be considered to be "mini axon hillocks", as their purpose is to boost the signal in order to prevent significant signal decay. At the furthest end, the axon loses its insulation and begins to branch into several [[axon terminal]]s. These presynaptic terminals, or synaptic boutons, are a specialized area within the axon of the presynaptic cell that contains [[neurotransmitters]] enclosed in small membrane-bound spheres called [[synaptic vesicle]]s.
神经元是由一个或多个树突、一个体细胞、一个轴突和一个或多个轴突终末组成的电激活细胞。树突是细胞的投射，其主要功能是接收突触信号。它们的突起被称为树突棘，用来捕获突触前神经元释放的神经递质。它们具有高浓度的配体门控离子通道。这些棘有一个细细的颈部，连接球状突起和树突。这确保脊柱内部发生的变化不太可能影响邻近的脊柱。树突棘除了极少数例外(见 LTP) ，可以作为一个独立的单位。树突从细胞体延伸出来，细胞体是细胞核和许多“正常”的真核细胞器的所在地。与脊柱不同，躯体的表面布满了电压激活的离子通道。这些通道帮助传输由树突产生的信号。从躯体出来的是轴突岗。这个区域有一个非常高浓度的电压激活钠离子通道拥有属性。一般认为它是动作电位的尖峰起始区。触发区。在脊柱处产生的多个信号，由躯体传输的信号都在这里汇聚。紧跟在轴突岗之后的是轴突。这是一个细管状突起，从躯体中游离出来。轴突由髓鞘绝缘。髓鞘由施万细胞(周围神经系统)或少突胶质细胞(中枢神经系统)组成，这两种细胞都是神经胶质细胞。虽然神经胶质细胞不参与电信号的传递，但它们可以相互沟通，为神经元提供重要的生化支持。具体来说，髓磷脂在轴突周围多次包裹，形成一层厚厚的脂肪层，阻止离子进入或逃离轴突。这种绝缘防止显着的信号衰减，以及确保更快的信号速度。然而，这种绝缘有一个限制，即轴突表面不能有通道。因此，有规则间隔的膜片，没有绝缘层。这些郎飞结可以被认为是“迷你轴突小丘”，因为他们的目的是增强信号，以防止重大信号衰减。在最远端，轴突失去了它的绝缘性，并开始分支成几个轴突终端。这些突触前终末，或称突触终结，是突触前细胞轴突内的一个特殊区域，其中包含神经递质，这些神经递质被包裹在被称为突触小泡的小膜内。
神经元是由一个或多个树突、一个体细胞、一个轴突和一个或多个轴突终末组成的电激活细胞。树突是细胞的投射，其主要功能是接收突触信号。它们的突起被称为树突棘，用来捕获突触前神经元释放的神经递质。它们具有高浓度的配体门控离子通道。这些棘有一个细细的颈部，连接球状突起和树突。这确保脊柱内部发生的变化不太可能影响邻近的脊柱。树突棘除了极少数例外(见 LTP) ，可以作为一个独立的单位。树突从细胞体延伸出来，细胞体是细胞核和许多“正常”的真核细胞器的所在地。与脊柱不同，躯体的表面布满了电压激活的离子通道。这些通道帮助传输由树突产生的信号。从躯体出来的是轴突岗。这个区域有一个非常高浓度的电压激活钠离子通道拥有属性。一般认为它是动作电位的尖峰起始区。触发区。在脊柱处产生的多个信号，由躯体传输的信号都在这里汇聚。紧跟在轴突岗之后的是轴突。这是一个细管状突起，从躯体中游离出来。轴突由髓鞘绝缘。髓鞘由施万细胞(周围神经系统)或少突胶质细胞(中枢神经系统)组成，这两种细胞都是神经胶质细胞。虽然神经胶质细胞不参与电信号的传递，但它们可以相互沟通，为神经元提供重要的生化支持。具体来说，髓磷脂在轴突周围多次包裹，形成一层厚厚的脂肪层，阻止离子进入或逃离轴突。这种绝缘防止显着的信号衰减，以及确保更快的信号速度。然而，这种绝缘有一个限制，即轴突表面不能有通道。因此，有规则间隔的膜片，没有绝缘层。这些郎飞结可以被认为是“迷你轴突小丘”，因为他们的目的是增强信号，以防止重大信号衰减。在最远端，轴突失去了它的绝缘性，并开始分支成几个轴突终端。这些突触前终末，或称突触终结，是突触前细胞轴突内的一个特殊区域，其中包含神经递质，这些神经递质被包裹在被称为突触小泡的小膜内。
===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. 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.
当动作电位到达突触前轴突（上）的末端时，它会导致神经递质分子的释放，这些分子打开突触后神经元中的离子通道（底部）。这些输入的兴奋性和抑制性突触后电位的组合可以在突触后神经元中开始新的动作电位。|链接=Special:FilePath/SynapseSchematic_en.svg]]
在考虑动作电位沿轴突的传播及其在突触结节的终止之前，有必要考虑一下在轴突突起处引发动作电位的方法。最基本的要求就是把山岗上的膜电位抬高到射击的门槛以上。有几种方式可以发生这种去极化。
在考虑动作电位沿轴突的传播及其在突触结节的终止之前，有必要考虑一下在轴突突起处引发动作电位的方法。最基本的要求就是把山岗上的膜电位抬高到射击的门槛以上。有几种方式可以发生这种去极化。
===Pacemaker potentials===
===Pacemaker potentials===
{{Main|Pacemaker potential}}
{{Main|Pacemaker potential}}
[[文件:Pacemaker potential.svg.png|替代=|缩略图|In [[pacemaker potential]]s, the cell spontaneously depolarizes (straight line with upward slope) until it fires an action potential.]]
[[文件:Pacemaker potential.svg.png|替代=|缩略图|In [[pacemaker potential]]s, the cell spontaneously depolarizes (straight line with upward slope) until it fires an action potential.
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 起搏器电位s中，细胞自发地去极化（具有向上斜率的直线），直到它发射动作电位。]]
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. The voltage traces of such cells are known as [[pacemaker potential]]s. 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. The external stimuli do not cause the cell's repetitive firing, but merely alter its timing. 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。
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。
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。
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.
比较猫中髓鞘和无髓鞘轴突s的传导速度。模板：Sfn 髓鞘神经元的传导速度 v 与轴突直径 d（即 v ∝ d）大致呈线性变化，[lower-alpha 1] 而无髓鞘神经元的速度大致与平方根 （v ∝模板：Radic） 一样变化。[下阿尔法2]红色和蓝色曲线是实验数据的拟合，而虚线是它们的理论推断。|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 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 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>
==Other cell types 其他细胞类型==
==Other cell types 其他细胞类型==
===Cardiac action potentials 心肌动作电位===
===Cardiac action potentials 心肌动作电位===
[[Image:Ventricular myocyte action potential.svg|thumb|220px|[[文件:Ventricular myocyte action potential.svg.png|缩略图]]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.png|替代=]]
[[Image:Ventricular myocyte action potential.svg|thumb|220px|[[文件:Ventricular myocyte action potential.svg.png|缩略图]]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.
心脏动作电位的阶段。电压的急剧上升（“0”）对应于钠离子的流入，而两个衰变（分别为“1”和“3”）对应于钠通道失活和钾离子的再极化流。特征性平台（“2”）是由电压敏感钙通道的打开引起的。|链接=Special:FilePath/Ventricular_myocyte_action_potential.svg.png]]
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.
==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>长鳍近海鱿鱼（Doryteuthis pealeii）的巨型轴突对于科学家了解动作潜力至关重要。[注1]|链接=Special:FilePath/Loligo_forbesii.jpg]]
The study of action potentials has required the development of new experimental methods. The initial work, prior to 1955, was carried out primarily by [[Alan Lloyd Hodgkin]] and [[Andrew Fielding Huxley]], who were, along [[John Carew Eccles]], awarded the 1963 [[Nobel Prize in Physiology or Medicine]] for their contribution to the description of the ionic basis of nerve conduction. It focused on three goals: isolating signals from single neurons or axons, developing fast, sensitive electronics, and shrinking [[electrode]]s enough that the voltage inside a single cell could be recorded.
The study of action potentials has required the development of new experimental methods. The initial work, prior to 1955, was carried out primarily by [[Alan Lloyd Hodgkin]] and [[Andrew Fielding Huxley]], who were, along [[John Carew Eccles]], awarded the 1963 [[Nobel Prize in Physiology or Medicine]] for their contribution to the description of the ionic basis of nerve conduction. It focused on three goals: isolating signals from single neurons or axons, developing fast, sensitive electronics, and shrinking [[electrode]]s enough that the voltage inside a single cell could be recorded.
==History历史==
==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.
两个浦肯野细胞的图像（标记为'''A'''），由圣地亚哥·拉蒙·卡哈尔于1899年绘制。大树状树状的树状物进入索玛，从中出现单个轴突，并通常向下移动，并带有几个分支点。标记B的较小细胞 是颗粒细胞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>
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。
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.
钠钾泵在其E2-Pi状态下的带状图。脂质双层的估计边界显示为蓝色（细胞内）和红色（细胞外）平面。|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" 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>
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>
==Quantitative models==
==Quantitative models==
[[Image:MembraneCircuit.svg|thumb|336px|right|Equivalent electrical circuit for the Hodgkin–Huxley model of the action potential. ''I<sub>m</sub>'' and ''V<sub>m</sub>'' represent the current through, and the voltage across, a small patch of membrane, respectively. The ''C<sub>m</sub>'' 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<sub>m</sub>'' and ''V<sub>m</sub>'' represent the current through, and the voltage across, a small patch of membrane, respectively. The ''C<sub>m</sub>'' 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]].
作用电位的霍奇金-赫胥黎模型的等效电路。''I<sub>m</sub>'' 和 ''V<sub>m</sub>'' 分别表示通过一小块膜的电流和两端的电压。''C<sub>m</sub>''代表膜贴片的电容，而四''g''代表四种离子的电导率。左边的两个电导，钾（K）和钠（Na），用箭头显示，表明它们可以随着施加的电压而变化，对应于电压敏感的离子通道。右侧的两个电导有助于确定静息膜电位。|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 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>
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>