动作电位

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As an action potential (nerve impulse) travels down an axon there is a change in polarity across the membrane of the axon. In response to a signal from another neuron, sodium- (Na⁺) and potassium- (K⁺) gated ion channels open and close as the membrane reaches its threshold potential. Na⁺ channels open at the beginning of the action potential, and Na⁺ moves into the axon, causing depolarization. Repolarization occurs when the K⁺ channels open and K⁺ moves out of the axon, creating a change in polarity between the outside of the cell and the inside. The impulse travels down the axon in one direction only, to the axon terminal where it signals other neurons.

In physiology, an action potential (AP) occurs when the membrane potential of a specific cell location rapidly rises and falls: this depolarization then causes adjacent locations to similarly depolarize. Action potentials occur in several types of animal cells, called excitable cells, which include neurons, muscle cells, endocrine cells and in some plant cells.

In physiology, an action potential (AP) occurs when the membrane potential of a specific cell location rapidly rises and falls: this depolarization then causes adjacent locations to similarly depolarize. Action potentials occur in several types of animal cells, called excitable cells, which include neurons, muscle cells, endocrine cells and in some plant cells.

在生理学上，当某个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) : 这种去极化会导致相邻部位同样的去极化。动作电位发生在几种类型的动物细胞，称为兴奋细胞，其中包括神经元，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-to-cell communication by providing for—or with regard to saltatory conduction, assisting—the propagation of signals along the neuron's axon toward 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 cells of the pancreas, they provoke release of insulin. Action potentials in neurons are also known as "nerve impulses" or "spikes", and the temporal sequence of action potentials generated by a neuron is called its "spike train". A neuron that emits an action potential, or nerve impulse, is often said to "fire".

In neurons, action potentials play a central role in cell-to-cell communication by providing for—or with regard to saltatory conduction, assisting—the propagation of signals along the neuron's axon toward 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 cells of the pancreas, they provoke release of insulin. 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".

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点传播; 这些信号然后可以与突触中的其他神经元连接，或与运动细胞或腺体连接。在其他类型的细胞中，它们的主要功能是激活细胞内的进程。例如，在肌肉细胞中，动作电位是导致肌肉收缩的一系列事件中的第一步。在胰腺的 β 细胞中，它们会刺激胰岛素的释放。神经元中的动作电位也被称为“神经冲动”或“尖峰”，神经元产生的动作电位的时间序列被称为“尖峰列车”。发出动作电位或神经冲动的神经元，通常被称为“发射”。

Action potentials are generated by special types of voltage-gated ion channels embedded in a cell's plasma membrane. 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, depolarising the transmembrane potential. When the channels open, they allow an inward flow of sodium ions, which changes the electrochemical gradient, which in turn produces a further rise in the membrane potential towards zero. This then causes more channels to open, producing a greater electric current across the cell membrane and so on. The process proceeds explosively until all of the available ion channels are open, resulting in a large upswing in the membrane potential. The rapid influx of sodium ions causes the polarity of the plasma membrane to reverse, and the ion channels then rapidly inactivate. As the sodium channels close, sodium ions can no longer enter the neuron, and they are then actively transported back out of the plasma membrane. Potassium channels are then activated, and there is an outward current of potassium ions, returning the electrochemical gradient to the resting state. After an action potential has occurred, there is a transient negative shift, called the afterhyperpolarization.

Action potentials are generated by special types of voltage-gated ion channels embedded in a cell's plasma membrane. 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, depolarising the transmembrane potential. 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。当膜电位接近细胞的负静息电位时，这些通道就会关闭，但是如果膜电位增加到一个精确定义的阈值电压，它们就会迅速开启，从而使膜电位去偏。当通道打开时，它们允许钠离子向内流动，这改变了电化梯度，反过来又使膜电位进一步升高到零。这就导致更多的通道打开，在细胞膜上产生更大的电流等等。这个过程爆炸性地进行，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。钠离子的快速注入导致质膜极性反转，离子通道迅速失活。随着钠离子通道的关闭，钠离子不能再进入神经元，然后它们被主动地从质膜中运输回来。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，有一瞬间的负移动，称为后超极化。

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. In some types of neurons, slow calcium spikes provide the driving force for a long burst of rapidly emitted sodium spikes. In 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.

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. In some types of neurons, slow calcium spikes provide the driving force for a long burst of rapidly emitted sodium spikes. In 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.

在动物细胞中，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。钠基动作电位通常持续不到一毫秒，但钙基动作电位可能持续100毫秒或更长时间。在某些类型的神经元中，缓慢的钙峰提供了快速释放钠峰的长时间爆发的驱动力。另一方面，在心肌细胞中，一个初始的快速钠峰提供了一个“引物”来激发钙峰的快速发作，然后产生肌肉收缩。

Overview

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.

Nearly all cell membranes 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 neurons 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.

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. Nearly all cell membranes 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 neurons 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.

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。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。

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 channels.

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 channels.

细胞的电特性是由细胞周围的膜的结构决定的。细胞膜由一层类脂双分子层组成，其中包含较大的蛋白质分子。这种类脂双分子层对带电离子的运动具有很强的抵抗力，因此它起到了绝缘体的作用。相比之下，大型膜内蛋白质提供离子通过的通道。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部和外部电压差的变化在闭合状态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

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.

All cells in animal body tissues are 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 pumps and ion channels. In neurons, the types of ion channels in the membrane usually vary across different parts of the cell, giving the dendrites, axon, and 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.

All cells in animal body tissues are 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 pumps and ion channels. In neurons, the types of ion channels in the membrane usually vary across different parts of the cell, giving the dendrites, axon, and 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.

= = = 一个典型神经元的过程 = = = 动物体组织中的所有细胞都是电极化的——换句话说，它们在细胞质膜上保持一个电压差，即所谓的膜电位。这种电极化是嵌入在膜中的蛋白质结构(称为离子泵和离子通道)之间复杂的相互作用的结果。在神经元中，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、轴突和细胞体具有不同的电特性。因此，神经元膜的某些部分可以被激活(能够产生动作电位) ，而其他部分则不能。近年来的研究表明，神经元最易兴奋的部位是轴突突起(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细胞体也易兴奋。

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 depolarize or hyperpolarize; that is, they cause the membrane potential to rise or fall. Action potentials are triggered when enough depolarization accumulates to bring the membrane potential up to threshold. When an action potential is triggered, the membrane potential abruptly shoots upward and then equally abruptly shoots back downward, often ending below the resting level, where it remains for some period of time. The shape of the action potential is stereotyped; this means that the rise and fall usually have approximately the same amplitude and time course for all action potentials in a given cell. (Exceptions are discussed later in the article). In most neurons, the entire process takes place in about a thousandth of a second. Many types of neurons emit action potentials constantly at rates of up to 10–100 per second. However, some types are much quieter, and may go for minutes or longer without emitting any action potentials.

Each excitable patch of membrane has two important levels of membrane potential: the resting potential, which is the value the membrane potential maintains as long as nothing perturbs the cell, and a higher value called the threshold potential. At the axon hillock of a typical neuron, the resting potential is around –70 millivolts (mV) and the threshold potential is around –55 mV. Synaptic inputs to a neuron cause the membrane to depolarize or 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，这是膜电位维持的值，只要没有什么干扰细胞，和一个更高的值称为阈值电位。在典型神经元的轴突丘，静息电位电位约为 -70毫伏，阈值电位约为 -55毫伏。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，膜电位突然向上发射，然后同样突然向下发射，通常在休息水平以下结束，在休息水平保持一段时间。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的速度发出动作电位。然而，有些类型更安静，可能持续几分钟或更长时间而不发出任何动作电位。

Biophysical basis

Action potentials result from the presence in a cell's membrane of special types of voltage-gated ion channels. A voltage-gated ion channel is a transmembrane protein that has three key properties:

1. It is capable of assuming more than one conformation.
2. At least one of the conformations creates a channel through the membrane that is permeable to specific types of ions.
3. The transition between conformations is influenced by the membrane potential.

Action potentials result from the presence in a cell's membrane of special types of voltage-gated ion channels. A voltage-gated ion channel is a transmembrane protein that has three key properties:

1. It is capable of assuming more than one conformation.
2. At least one of the conformations creates a channel through the membrane that is permeable to specific types of ions.
3. 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。电压门控离子通道是一种跨膜蛋白，有3个关键属性: # 它能够承担多个构象。# 至少其中一种构象在膜上形成一个通道，可以渗透特定种类的离子。# 构象之间的转换受到膜电位的影响。

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.

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价值倾向于开放，而对其他价值倾向于关闭。然而，在大多数情况下，膜电位和信道状态之间的关系是概率的，并且包含一个时间延迟。离子通道在不可预知的时间里在不同构象之间切换: 膜电位分子理论决定了每种类型的跃迁的速率和单位时间的概率。

Action potential propagation along an axon

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 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.

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。当这种正反馈周期(霍奇金周期)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态。

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

The most intensively studied type of voltage-dependent ion channels comprises the sodium channels involved in fast nerve conduction. These are sometimes known as Hodgkin-Huxley sodium channels because they were first characterized by Alan 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 NaV channels. (The "V" stands for "voltage".) An NaV 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生物物理学研究中的第一个拥有属性，但是更方便地被称为 NaV 通道。(“ v”代表“电压”。)导航通道有三种可能的状态，被称为失活、激活和失活。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，通道显示过渡到激活(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，通道最终会过渡到灭活状态。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停止→激活→灭活→停止的过程。这只是种群平均行为，然而——一个个体渠道原则上可以在任何时间进行任何转换。然而，通道从灭活状态直接过渡到活化状态的可能性非常低: 处于灭活状态的通道是难熔的，直到它回到灭活状态。

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

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

Ion movement during an action potential.
Key: a) Sodium (Na⁺) ion. b) Potassium (K⁺) ion. c) Sodium channel. d) Potassium channel. e) Sodium-potassium pump.
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 inactivated while the Na⁺ and K⁺ ions return to their resting state distributions across the membrane (1), and the neuron is ready to repeat the process for the next action potential.

模板:AnchorAs the membrane potential is increased, sodium ion channels open, allowing the entry of sodium ions into the cell. This is followed by the opening of 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 cations 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.模板:Sfn模板:Sfn模板:Sfn 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.模板:Sfn模板:Sfnm模板:Sfn模板:Refn The frequency at which a neuron elicits action potentials is often referred to as a firing rate or neural firing rate.

As the membrane potential is increased, sodium ion channels open, allowing the entry of sodium ions into the cell. This is followed by the opening of 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 cations 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. 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. The frequency at which a neuron elicits action potentials is often referred to as a firing rate or neural firing rate.

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

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-nothing property of the action potential sets it apart from graded potentials such as receptor potentials, electrotonic potentials, subthreshold membrane potential oscillations, and synaptic potentials, which scale with the magnitude of the stimulus. A variety of action potential types exist in many cell types and cell compartments as determined by the types of voltage-gated channels, leak channels, channel distributions, ionic concentrations, membrane capacitance, temperature, and other factors.

Currents produced by the opening of voltage-gated channels in the course of an action potential are typically significantly larger than the initial stimulating current. Thus, the amplitude, duration, and shape of the action potential are determined largely by the properties of the excitable membrane and not the amplitude or duration of the stimulus. This all-or-nothing property of the action potential sets it apart from graded potentials such as receptor potentials, electrotonic potentials, subthreshold membrane potential oscillations, and synaptic potentials, 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。动作电位的这种全有或全无的特性使它有别于受体电位、电渗电位、阈下膜电位振荡和突触电位等随刺激强度变化的分级电位。根据电压门控通道的类型、漏通道、通道分布、离子浓度、膜电容、温度等因素的不同，许多细胞类型和细胞腔室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 transporters, maintains the normal ratio of ion concentrations across the membrane. Calcium cations and chloride anions are involved in a few types of action potentials, such as the cardiac action potential and the action potential in the single-cell alga Acetabularia, respectively.

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

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

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. 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 terminals, in general, triggers the release of neurotransmitter into the synaptic cleft. In addition, backpropagating action potentials have been recorded in the dendrites of pyramidal neurons, which are ubiquitous in the neocortex. These are thought to have a role in spike-timing-dependent plasticity.

Although action potentials are generated locally on patches of excitable membrane, the resulting currents can trigger action potentials on neighboring stretches of membrane, precipitating a domino-like propagation. In contrast to passive spread of electric potentials (electrotonic potential), action potentials are generated anew along excitable stretches of membrane and propagate without decay.Schmidt-Nielsen, p. 484. 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 terminals, in general, triggers the release of neurotransmitter into the synaptic cleft. In addition, backpropagating action potentials have been recorded in the dendrites of pyramidal neurons, which are ubiquitous in the neocortex. These are thought to have a role in spike-timing-dependent plasticity.

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

In the 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. Moreover, contradictory measurements of entropy changes and timing disputed the capacitance model as acting alone. 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.

In the 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. Moreover, contradictory measurements of entropy changes and timing disputed the capacitance model as acting alone. 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.

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

Maturation of the electrical properties of the action potential

A neuron's ability to generate and propagate an action potential changes during development. How much the membrane potential of a neuron changes as the result of a current impulse is a function of the membrane input resistance. As a cell grows, more 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. 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.

A neuron's ability to generate and propagate an action potential changes during development. How much the membrane potential of a neuron changes as the result of a current impulse is a function of the membrane input resistance. As a cell grows, more 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. 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.

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

In the early development of many organisms, the action potential is actually initially carried by calcium current rather than sodium current. The 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. 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 inward current becomes primarily carried by sodium channels. Second, the delayed rectifier, a potassium channel current, increases to 3.5 times its initial strength.

In the early development of many organisms, the action potential is actually initially carried by calcium current rather than sodium current. The 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. 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 inward current becomes primarily carried by sodium channels. Second, the delayed rectifier, a potassium channel current, increases to 3.5 times its initial strength.

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

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 RNA synthesis or protein synthesis inhibitors that transition is prevented. Even the electrical activity of the cell itself may play a role in channel expression. If action potentials in Xenopus myocytes are blocked, the typical increase in sodium and potassium current density is prevented or delayed.

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 RNA synthesis or protein synthesis inhibitors that transition is prevented. Even the electrical activity of the cell itself may play a role in channel expression. If action potentials in Xenopus myocytes are blocked, the typical increase in sodium and potassium current density is prevented or delayed.

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

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 cortical neurons increases by 600% within the first two postnatal weeks.

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 cortical neurons increases by 600% within the first two postnatal weeks.

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

Neurotransmission

Main article: Neurotransmission

Anatomy of a neuron

模板:Neuron map 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。

Neurons are electrically excitable cells composed, in general, of one or more dendrites, a single soma, a single axon and one or more axon terminals. Dendrites are cellular projections whose primary function is to receive synaptic signals. Their protrusions, known as dendritic spines, are designed to capture the neurotransmitters released by the presynaptic neuron. They have a high concentration of ligand-gated ion channels. 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 LTP), act as an independent unit. The dendrites extend from the soma, which houses the nucleus, and many of the "normal" 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,模板:Sfn 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.模板:Sfn 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 terminals. 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 vesicles.

Neurons are electrically excitable cells composed, in general, of one or more dendrites, a single soma, a single axon and one or more axon terminals. Dendrites are cellular projections whose primary function is to receive synaptic signals. Their protrusions, known as dendritic spines, are designed to capture the neurotransmitters released by the presynaptic neuron. They have a high concentration of ligand-gated ion channels. 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 LTP), act as an independent unit. The dendrites extend from the soma, which houses the nucleus, and many of the "normal" 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 terminals. 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 vesicles.

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

Before considering the propagation of action potentials along axons 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.模板:Sfn模板:Sfn模板:Sfnm模板:Sfn There are several ways in which this depolarization can occur.

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 and inhibitory postsynaptic potentials of such inputs can begin a new action potential in the post-synaptic neuron.

Before considering the propagation of action potentials along axons 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.

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。

Dynamics

Action potentials are most commonly initiated by excitatory postsynaptic potentials from a presynaptic neuron.模板:Sfnm Typically, neurotransmitter molecules are released by the presynaptic neuron. These neurotransmitters then bind to receptors on the postsynaptic cell. This binding opens various types of ion channels. This opening has the further effect of changing the local permeability of the cell membrane and, thus, the membrane potential. If the binding increases the voltage (depolarizes the membrane), the synapse is excitatory. If, however, the binding decreases the voltage (hyperpolarizes the membrane), it is inhibitory. Whether the voltage is increased or decreased, the change propagates passively to nearby regions of the membrane (as described by the cable equation and its refinements). Typically, the voltage stimulus decays exponentially with the distance from the synapse and with time from the binding of the neurotransmitter. Some fraction of an excitatory voltage may reach the axon hillock and may (in rare cases) depolarize the membrane enough to provoke a new action potential. More typically, the excitatory potentials from several synapses must work together at nearly the same time to provoke a new action potential. Their joint efforts can be thwarted, however, by the counteracting inhibitory postsynaptic potentials.

Action potentials are most commonly initiated by excitatory postsynaptic potentials from a presynaptic neuron. Typically, neurotransmitter molecules are released by the presynaptic neuron. These neurotransmitters then bind to receptors on the postsynaptic cell. This binding opens various types of ion channels. This opening has the further effect of changing the local permeability of the cell membrane and, thus, the membrane potential. If the binding increases the voltage (depolarizes the membrane), the synapse is excitatory. If, however, the binding decreases the voltage (hyperpolarizes the membrane), it is inhibitory. Whether the voltage is increased or decreased, the change propagates passively to nearby regions of the membrane (as described by the cable equation and its refinements). Typically, the voltage stimulus decays exponentially with the distance from the synapse and with time from the binding of the neurotransmitter. Some fraction of an excitatory voltage may reach the axon hillock and may (in rare cases) depolarize the membrane enough to provoke a new action potential. More typically, the excitatory potentials from several synapses must work together at nearly the same time to provoke a new action potential. Their joint efforts can be thwarted, however, by the counteracting inhibitory postsynaptic potentials.

动作电位通常由突触前神经元的兴奋性突触后电位引起。通常，神经递质分子由突触前神经元释放。这些神经递质随后与突触后细胞上的受体结合。这种结合打开了各种类型的离子通道。这个开口具有改变细胞膜局部通透性的进一步效果，从而改变了膜电位的通透性。如果结合增加电压(去极化膜) ，突触是兴奋性的。然而，如果这种结合降低了电压(使细胞膜超极化) ，它就是抑制。无论电压是升高还是降低，这种变化都会被动地传播到膜的附近区域(如电缆方程及其改进所描述的)。通常情况下，电压刺激随着与突触的距离和与神经递质结合的时间成指数衰减。兴奋性电压的一部分可能到达轴突小丘，并且(在少数情况下)使膜去极化，足以引起新的动作电位。更典型的是，来自几个突触的兴奋性电位必须在几乎同一时间共同激发一个新的动作电位。然而，他们的共同努力可能被反作用的抑制性突触后电位所阻碍。

Neurotransmission can also occur through electrical synapses.模板:Sfnm Due to the direct connection between excitable cells in the form of gap junctions, an action potential can be transmitted directly from one cell to the next in either direction. The free flow of ions between cells enables rapid non-chemical-mediated transmission. Rectifying channels ensure that action potentials move only in one direction through an electrical synapse. Electrical synapses are found in all nervous systems, including the human brain, although they are a distinct minority.模板:Sfn

Neurotransmission can also occur through electrical synapses. Due to the direct connection between excitable cells in the form of gap junctions, an action potential can be transmitted directly from one cell to the next in either direction. The free flow of ions between cells enables rapid non-chemical-mediated transmission. Rectifying channels ensure that action potentials move only in one direction through an electrical synapse. Electrical synapses are found in all nervous systems, including the human brain, although they are a distinct minority.

神经传导也可以通过电突触发生。由于可兴奋细胞之间以缝隙连接的形式存在直接联系，动作电位可以从一个细胞直接传递到下一个细胞。离子在细胞之间的自由流动使得非化学介导的快速传输成为可能。整流通道确保动作电位通过电突触向一个方向移动。电突触存在于所有神经系统中，包括人脑，尽管它们只是少数。

"All-or-none" principle

Main article: All-or-none law

The amplitude of an action potential is independent of the amount of current that produced it. In other words, larger currents do not create larger action potentials. Therefore, action potentials are said to be all-or-none signals, since either they occur fully or they do not occur at all. This is in contrast to receptor potentials, whose amplitudes are dependent on the intensity of a stimulus.模板:Sfn In both cases, the frequency of action potentials is correlated with the intensity of a stimulus.

The amplitude of an action potential is independent of the amount of current that produced it. In other words, larger currents do not create larger action potentials. Therefore, action potentials are said to be all-or-none signals, since either they occur fully or they do not occur at all.Sasaki, T., Matsuki, N., Ikegaya, Y. 2011 Action-potential modulation during axonal conduction Science 331 (6017), pp. 599–601Aur D., Jog, MS., 2010 Neuroelectrodynamics: Understanding the brain language, IOS Press, 2010. This is in contrast to receptor potentials, whose amplitudes are dependent on the intensity of a stimulus. In both cases, the frequency of action potentials is correlated with the intensity of a stimulus.

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

Sensory neurons

Main article: Sensory neuron

In sensory neurons, an external signal such as pressure, temperature, light, or sound is coupled with the opening and closing of ion channels, which in turn alter the ionic permeabilities of the membrane and its voltage.模板:Sfnm These voltage changes can again be excitatory (depolarizing) or inhibitory (hyperpolarizing) and, in some sensory neurons, their combined effects can depolarize the axon hillock enough to provoke action potentials. Some examples in humans include the olfactory receptor neuron and Meissner's corpuscle, which are critical for the sense of smell and touch, respectively. However, not all sensory neurons convert their external signals into action potentials; some do not even have an axon.模板:Sfnm Instead, they may convert the signal into the release of a neurotransmitter, or into continuous graded potentials, either of which may stimulate subsequent neuron(s) into firing an action potential. For illustration, in the human ear, hair cells convert the incoming sound into the opening and closing of mechanically gated ion channels, which may cause neurotransmitter molecules to be released. In similar manner, in the human retina, the initial photoreceptor cells and the next layer of cells (comprising bipolar cells and horizontal cells) do not produce action potentials; only some amacrine cells and the third layer, the ganglion cells, produce action potentials, which then travel up the optic nerve.

In sensory neurons, an external signal such as pressure, temperature, light, or sound is coupled with the opening and closing of ion channels, which in turn alter the ionic permeabilities of the membrane and its voltage. These voltage changes can again be excitatory (depolarizing) or inhibitory (hyperpolarizing) and, in some sensory neurons, their combined effects can depolarize the axon hillock enough to provoke action potentials. Some examples in humans include the olfactory receptor neuron and Meissner's corpuscle, which are critical for the sense of smell and touch, respectively. However, not all sensory neurons convert their external signals into action potentials; some do not even have an axon. Instead, they may convert the signal into the release of a neurotransmitter, or into continuous graded potentials, either of which may stimulate subsequent neuron(s) into firing an action potential. For illustration, in the human ear, hair cells convert the incoming sound into the opening and closing of mechanically gated ion channels, which may cause neurotransmitter molecules to be released. In similar manner, in the human retina, the initial photoreceptor cells and the next layer of cells (comprising bipolar cells and horizontal cells) do not produce action potentials; only some amacrine cells and the third layer, the ganglion cells, produce action potentials, which then travel up the optic nerve.

在感觉神经元中，外部信号如压力、温度、光或声音与离子通道的开启和关闭相耦合，这反过来又改变了膜的离子通透性及其电压。这些电压变化可以是兴奋性(去极化)或抑制性(超极化) ，在某些感觉神经元中，它们的联合作用可以使轴突丘去极化，足以激发动作电位。人类的一些例子包括嗅觉受器神经元和迈斯纳氏小体，它们分别对嗅觉和触觉至关重要。然而，并不是所有的感觉神经元都将外部信号转换成动作电位，有些甚至没有轴突。相反，他们可以将信号转换成一种神经递质的释放，或者转换成连续分级的电位，这两种电位都可以刺激后续的神经元发出动作电位。例如，在人耳中，毛细胞将传入的声音转换成机械门控离子通道的开闭，这可能导致神经递质分子的释放。同样，在人类视网膜中，最初的感光细胞和下一层细胞(包括双极细胞和水平细胞)不产生动作电位，只有一些无长突细胞和第三层神经节细胞产生动作电位，然后动作电位沿视神经传递。

Pacemaker potentials

Main article: Pacemaker potential

In pacemaker potentials, 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.模板:Sfn The voltage traces of such cells are known as pacemaker potentials.模板:Sfn The cardiac pacemaker cells of the sinoatrial node in the heart provide a good example. Although such pacemaker potentials have a 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 and parasympathetic nerves.模板:Sfn The external stimuli do not cause the cell's repetitive firing, but merely alter its timing.模板:Sfn In some cases, the regulation of frequency can be more complex, leading to patterns of action potentials, such as bursting.

In sensory neurons, action potentials result from an external stimulus. However, some excitable cells require no such stimulus to fire: They spontaneously depolarize their axon hillock and fire action potentials at a regular rate, like an internal clock. The voltage traces of such cells are known as pacemaker potentials. The cardiac pacemaker cells of the sinoatrial node in the heart provide a good example. Although such pacemaker potentials have a 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 and 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。虽然这种起搏器电位具有自然节律，但它可以通过外部刺激进行调节; 例如，药物以及交感神经和副交感神经发出的信号可以改变心率。外部刺激不会引起细胞的反复放电，只是改变了它的放电时间。在某些情况下，频率的调节可能更加复杂，导致动作电位的模式，如爆发。

Phases

The course of the action potential can be divided into five parts: the rising phase, the peak phase, the falling phase, the undershoot phase, and the refractory period. During the rising phase the membrane potential depolarizes (becomes more positive). The point at which depolarization stops is called the peak phase. At this stage, the membrane potential reaches a maximum. Subsequent to this, there is a falling phase. During this stage the membrane potential becomes more negative, returning towards resting potential. The undershoot, or afterhyperpolarization, phase is the period during which the membrane potential temporarily becomes more negatively charged than when at rest (hyperpolarized). Finally, the time during which a subsequent action potential is impossible or difficult to fire is called the refractory period, which may overlap with the other phases.模板:Sfn

The course of the action potential can be divided into five parts: the rising phase, the peak phase, the falling phase, the undershoot phase, and the refractory period. During the rising phase the membrane potential depolarizes (becomes more positive). The point at which depolarization stops is called the peak phase. At this stage, the membrane potential reaches a maximum. Subsequent to this, there is a falling phase. During this stage the membrane potential becomes more negative, returning towards resting potential. The undershoot, or afterhyperpolarization, phase is the period during which the membrane potential temporarily becomes more negatively charged than when at rest (hyperpolarized). Finally, the time during which a subsequent action potential is impossible or difficult to fire is called the refractory period, which may overlap with the other phases.

动作电位的过程可分为上升期、峰值期、下降期、下冲期和不应期(性)。在上升阶段，膜电位去极化(变得更加积极)。退极化停止的点称为峰值相位。在这个阶段，膜电位达到了最大值。在这之后，有一个下降的阶段。在这个阶段，膜电位变得更加消极，回到了静息电位。下极化或后超极化阶段是膜电位暂时变得比静止时更加负极化的时期(超极化)。最后，不可能或难以触发随后的动作电位的时间被称为不应期(性) ，它可能与其他阶段重叠。

The course of the action potential is determined by two coupled effects.模板:Sfn First, voltage-sensitive ion channels open and close in response to changes in the membrane voltage V_m. This changes the membrane's permeability to those ions.模板:Sfn Second, according to the Goldman equation, this change in permeability changes the equilibrium potential E_m, and, thus, the membrane voltage V_m. Thus, the membrane potential affects the permeability, which then further affects the membrane potential. This sets up the possibility for positive feedback, which is a key part of the rising phase of the action potential.模板:Sfn模板:Sfnm A complicating factor is that a single ion channel may have multiple internal "gates" that respond to changes in V_m in opposite ways, or at different rates.模板:Sfnm For example, although raising V_m opens most gates in the voltage-sensitive sodium channel, it also closes the channel's "inactivation gate", albeit more slowly.模板:Sfnm Hence, when V_m is raised suddenly, the sodium channels open initially, but then close due to the slower inactivation.

The course of the action potential is determined by two coupled effects. First, voltage-sensitive ion channels open and close in response to changes in the membrane voltage Vm. This changes the membrane's permeability to those ions. Second, according to the Goldman equation, this change in permeability changes the equilibrium potential Em, and, thus, the membrane voltage Vm. Thus, the membrane potential affects the permeability, which then further affects the membrane potential. This sets up the possibility for positive feedback, which is a key part of the rising phase of the action potential. A complicating factor is that a single ion channel may have multiple internal "gates" that respond to changes in Vm in opposite ways, or at different rates. For example, although raising Vm opens most gates in the voltage-sensitive sodium channel, it also closes the channel's "inactivation gate", albeit more slowly. Hence, when Vm is raised suddenly, the sodium channels open initially, but then close due to the slower inactivation.

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

The voltages and currents of the action potential in all of its phases were modeled accurately by Alan Lloyd Hodgkin and Andrew Huxley in 1952, for which they were awarded the Nobel Prize in Physiology or Medicine in 1963. However, their model considers only two types of voltage-sensitive ion channels, and makes several assumptions about them, e.g., that their internal gates open and close independently of one another. In reality, there are many types of ion channels, and they do not always open and close independently.

The voltages and currents of the action potential in all of its phases were modeled accurately by Alan Lloyd Hodgkin and Andrew Huxley in 1952, for which they were awarded the Nobel Prize in Physiology or Medicine in 1963. However, their model considers only two types of voltage-sensitive ion channels, and makes several assumptions about them, e.g., that their internal gates open and close independently of one another. In reality, there are many types of ion channels,Goldin, AL in and they do not always open and close independently.

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

Stimulation and rising phase

A typical action potential begins at the axon hillock模板:Sfn with a sufficiently strong depolarization, e.g., a stimulus that increases V_m. This depolarization is often caused by the injection of extra sodium cations into the cell; these cations can come from a wide variety of sources, such as chemical synapses, sensory neurons or pacemaker potentials.

A typical action potential begins at the axon hillock with a sufficiently strong depolarization, e.g., a stimulus that increases Vm. This depolarization is often caused by the injection of extra sodium cations into the cell; these cations can come from a wide variety of sources, such as chemical synapses, sensory neurons or pacemaker potentials.

= = = 刺激和上升期 = = = 一个典型的动作电位开始于轴突丘，有足够强的去极化作用，例如，一个刺激增加了 Vm。这种去极化通常是由细胞注入额外的钠离子引起的; 这些阳离子可以来自多种来源，如化学突触、感觉神经元或起搏器电位。

For a neuron at rest, there is a high concentration of sodium and chloride ions in the extracellular fluid compared to the intracellular fluid, while there is a high concentration of potassium ions in the intracellular fluid compared to the extracellular fluid. The difference in concentrations, which causes ions to move from a high to a low concentration, and electrostatic effects (attraction of opposite charges) are responsible for the movement of ions in and out of the neuron. The inside of a neuron has a negative charge, relative to the cell exterior, from the movement of K⁺ out of the cell. The neuron membrane is more permeable to K⁺ than to other ions, allowing this ion to selectively move out of the cell, down its concentration gradient. This concentration gradient along with potassium leak channels present on the membrane of the neuron causes an efflux of potassium ions making the resting potential close to E_K ≈ –75 mV.模板:Sfnm Since Na⁺ ions are in higher concentrations outside of the cell, the concentration and voltage differences both drive them into the cell when Na⁺ channels open. Depolarization opens both the sodium and potassium channels in the membrane, allowing the ions to flow into and out of the axon, respectively. If the depolarization is small (say, increasing V_m from −70 mV to −60 mV), the outward potassium current overwhelms the inward sodium current and the membrane repolarizes back to its normal resting potential around −70 mV.模板:Sfn模板:Sfn模板:Sfn However, if the depolarization is large enough, the inward sodium current increases more than the outward potassium current and a runaway condition (positive feedback) results: the more inward current there is, the more V_m increases, which in turn further increases the inward current.模板:Sfn模板:Sfnm A sufficiently strong depolarization (increase in V_m) causes the voltage-sensitive sodium channels to open; the increasing permeability to sodium drives V_m closer to the sodium equilibrium voltage E_Na≈ +55 mV. The increasing voltage in turn causes even more sodium channels to open, which pushes V_m still further towards E_Na. This positive feedback continues until the sodium channels are fully open and V_m is close to E_Na.模板:Sfn模板:Sfn模板:Sfnm模板:Sfn The sharp rise in V_m and sodium permeability correspond to the rising phase of the action potential.模板:Sfn模板:Sfn模板:Sfnm模板:Sfn

For a neuron at rest, there is a high concentration of sodium and chloride ions in the extracellular fluid compared to the intracellular fluid, while there is a high concentration of potassium ions in the intracellular fluid compared to the extracellular fluid. The difference in concentrations, which causes ions to move from a high to a low concentration, and electrostatic effects (attraction of opposite charges) are responsible for the movement of ions in and out of the neuron. The inside of a neuron has a negative charge, relative to the cell exterior, from the movement of K+ out of the cell. The neuron membrane is more permeable to K+ than to other ions, allowing this ion to selectively move out of the cell, down its concentration gradient. This concentration gradient along with potassium leak channels present on the membrane of the neuron causes an efflux of potassium ions making the resting potential close to EK ≈ –75 mV. Since Na+ ions are in higher concentrations outside of the cell, the concentration and voltage differences both drive them into the cell when Na+ channels open. Depolarization opens both the sodium and potassium channels in the membrane, allowing the ions to flow into and out of the axon, respectively. If the depolarization is small (say, increasing Vm from −70 mV to −60 mV), the outward potassium current overwhelms the inward sodium current and the membrane repolarizes back to its normal resting potential around −70 mV. However, if the depolarization is large enough, the inward sodium current increases more than the outward potassium current and a runaway condition (positive feedback) results: the more inward current there is, the more Vm increases, which in turn further increases the inward current. A sufficiently strong depolarization (increase in Vm) causes the voltage-sensitive sodium channels to open; the increasing permeability to sodium drives Vm closer to the sodium equilibrium voltage ENa≈ +55 mV. The increasing voltage in turn causes even more sodium channels to open, which pushes Vm still further towards ENa. This positive feedback continues until the sodium channels are fully open and Vm is close to ENa. The sharp rise in Vm and sodium permeability correspond to the rising phase of the action potential.

对于处于静息状态的神经元来说，细胞外液中的钠离子和氯离子浓度高于细胞内液，而细胞内液中的钾离子浓度高于细胞外液。导致离子从高浓度移动到低浓度的浓度差，以及静电效应(相反电荷的吸引)是离子进出神经元的原因。神经元内部有一个负电荷，相对于细胞外部，来自于细胞外 k + 的运动。神经细胞膜比其他离子对 k + 的渗透性更强，使得这种离子能够选择性地离开细胞，沿着浓度梯度下降。这种浓度梯度以及神经元膜上的钾离子泄漏通道导致钾离子外流，使静息电位接近 EK ≈-75 mV。由于钠离子在细胞外的浓度较高，当钠离子通道打开时，浓度和电压的差异都驱使它们进入细胞。去极化打开了细胞膜上的钠通道和钾通道，允许离子分别流入和流出轴突。如果去极化很小(比如说，把 Vm 从 -70 mV 增加到 -60 mV) ，外向的钾电流压倒内向的钠电流，膜在 -70 mV 左右重新极化回正常的静息电位。然而，当退极化足够大时，内向钠电流的增加大于外向钾电流，出现了失控(正反馈)现象: 内向钠电流越大，内向钠电流越大，反过来又进一步增加内向钠电流。足够强的去极化(Vm 的增加)使电压敏感的钠通道开放，钠的渗透性增加使 Vm 接近钠平衡电压 ENa ≈ + 55 mV。增加的电压依次导致更多的钠离子通道打开，这使得 Vm 更靠近 ENa。这种正反馈持续到钠离子通道完全打开，Vm 接近 ENa。Vm 和钠通透性的急剧升高与动作电位的升高相对应。

The critical threshold voltage for this runaway condition is usually around −45 mV, but it depends on the recent activity of the axon. A cell that has just fired an action potential cannot fire another one immediately, since the Na⁺ channels have not recovered from the inactivated state. The period during which no new action potential can be fired is called the absolute refractory period.模板:Sfn模板:Sfn模板:Sfnm At longer times, after some but not all of the ion channels have recovered, the axon can be stimulated to produce another action potential, but with a higher threshold, requiring a much stronger depolarization, e.g., to −30 mV. The period during which action potentials are unusually difficult to evoke is called the relative refractory period.模板:Sfn模板:Sfn模板:Sfnm

The critical threshold voltage for this runaway condition is usually around −45 mV, but it depends on the recent activity of the axon. A cell that has just fired an action potential cannot fire another one immediately, since the Na+ channels have not recovered from the inactivated state. The period during which no new action potential can be fired is called the absolute refractory period. At longer times, after some but not all of the ion channels have recovered, the axon can be stimulated to produce another action potential, but with a higher threshold, requiring a much stronger depolarization, e.g., to −30 mV. The period during which action potentials are unusually difficult to evoke is called the relative refractory period.

这种失控状态的关键阈值电压通常在 -45 mV 左右，但这取决于轴突最近的活动。一个刚刚激发了动作电位的细胞不能立即激发另一个动作电位，因为 Na + 通道还没有从失活状态恢复过来。没有新的动作电位被激发的这段时间叫做绝对不应期(性)。在更长的时间里，当一些但不是全部的离子通道恢复后，轴突可以被刺激产生另一个动作电位，但是具有更高的阈值，需要更强的去极化，例如-30mv。动作电位异常难以唤起的时期称为相对不应期(性)。

Peak phase

The positive feedback of the rising phase slows and comes to a halt as the sodium ion channels become maximally open. At the peak of the action potential, the sodium permeability is maximized and the membrane voltage V_m is nearly equal to the sodium equilibrium voltage E_Na. However, the same raised voltage that opened the sodium channels initially also slowly shuts them off, by closing their pores; the sodium channels become inactivated.模板:Sfnm This lowers the membrane's permeability to sodium relative to potassium, driving the membrane voltage back towards the resting value. At the same time, the raised voltage opens voltage-sensitive potassium channels; the increase in the membrane's potassium permeability drives V_m towards E_K.模板:Sfnm Combined, these changes in sodium and potassium permeability cause V_m to drop quickly, repolarizing the membrane and producing the "falling phase" of the action potential.模板:Sfn模板:Sfn模板:Sfn模板:Sfnm

The positive feedback of the rising phase slows and comes to a halt as the sodium ion channels become maximally open. At the peak of the action potential, the sodium permeability is maximized and the membrane voltage Vm is nearly equal to the sodium equilibrium voltage ENa. However, the same raised voltage that opened the sodium channels initially also slowly shuts them off, by closing their pores; the sodium channels become inactivated. This lowers the membrane's permeability to sodium relative to potassium, driving the membrane voltage back towards the resting value. At the same time, the raised voltage opens voltage-sensitive potassium channels; the increase in the membrane's potassium permeability drives Vm towards EK. Combined, these changes in sodium and potassium permeability cause Vm to drop quickly, repolarizing the membrane and producing the "falling phase" of the action potential.

当钠离子通道最大程度地开放时，上升相的正反馈减慢并停止。在动作电位的峰值，钠离子的渗透性最大，膜电位的电压几乎等于钠离子的平衡电压 ENa。然而，最初打开钠离子通道的升高的电压也会通过关闭它们的毛孔而慢慢关闭它们; 钠离子通道变得不活跃。这降低了细胞膜相对于钾离子的钠离子通透性，使膜电位重新回到静息值。同时，升高的电压开启了电压敏感性钾离子通道，膜钾离子通透性的增加促使 Vm 向 EK 方向运动。这些钠和钾通透性的变化使 Vm 迅速下降，使膜再极化，产生动作电位的“下降相”。

Afterhyperpolarization

The depolarized voltage opens additional voltage-dependent potassium channels, and some of these do not close right away when the membrane returns to its normal resting voltage. In addition, further potassium channels open in response to the influx of calcium ions during the action potential. The intracellular concentration of potassium ions is transiently unusually low, making the membrane voltage V_m even closer to the potassium equilibrium voltage E_K. The membrane potential goes below the resting membrane potential. Hence, there is an undershoot or hyperpolarization, termed an afterhyperpolarization, that persists until the membrane potassium permeability returns to its usual value, restoring the membrane potential to the resting state.模板:Sfn模板:Sfn

The depolarized voltage opens additional voltage-dependent potassium channels, and some of these do not close right away when the membrane returns to its normal resting voltage. In addition, further potassium channels open in response to the influx of calcium ions during the action potential. The intracellular concentration of potassium ions is transiently unusually low, making the membrane voltage Vm even closer to the potassium equilibrium voltage EK. The membrane potential goes below the resting membrane potential. Hence, there is an undershoot or hyperpolarization, termed an afterhyperpolarization, that persists until the membrane potassium permeability returns to its usual value, restoring the membrane potential to the resting state.

= = = = 后超极化去极化电压开启了额外的电压依赖性钾离子通道，当膜恢复到正常的静息电压时，其中一些通道不会马上关闭。此外，在动作电位过程中，钙离子内流时，进一步的钾离子通道开放。细胞内钾离子浓度短暂地异常低，使膜电位向钾离子平衡电压更接近 EK。膜电位位于静止的膜电位下方。因此，存在一个被称为后超极化的超极化，持续到膜钾通透性恢复到正常值，恢复膜电位到静息状态。

Refractory period

Each action potential is followed by a refractory period, which can be divided into an absolute refractory period, during which it is impossible to evoke another action potential, and then a relative refractory period, during which a stronger-than-usual stimulus is required.模板:Sfn模板:Sfn模板:Sfnm These two refractory periods are caused by changes in the state of sodium and potassium channel molecules. When closing after an action potential, sodium channels enter an "inactivated" state, in which they cannot be made to open regardless of the membrane potential—this gives rise to the absolute refractory period. Even after a sufficient number of sodium channels have transitioned back to their resting state, it frequently happens that a fraction of potassium channels remains open, making it difficult for the membrane potential to depolarize, and thereby giving rise to the relative refractory period. Because the density and subtypes of potassium channels may differ greatly between different types of neurons, the duration of the relative refractory period is highly variable.

Each action potential is followed by a refractory period, which can be divided into an absolute refractory period, during which it is impossible to evoke another action potential, and then a relative refractory period, during which a stronger-than-usual stimulus is required. These two refractory periods are caused by changes in the state of sodium and potassium channel molecules. When closing after an action potential, sodium channels enter an "inactivated" state, in which they cannot be made to open regardless of the membrane potential—this gives rise to the absolute refractory period. Even after a sufficient number of sodium channels have transitioned back to their resting state, it frequently happens that a fraction of potassium channels remains open, making it difficult for the membrane potential to depolarize, and thereby giving rise to the relative refractory period. Because the density and subtypes of potassium channels may differ greatly between different types of neurons, the duration of the relative refractory period is highly variable.

= = = 每个动作电位后面跟着一个不应期(性) ，这个不应期(性)可以分为一个绝对不应期(性) ，在这个不应期(性)中不可能激发另一个动作电位，然后是一个相对的不应期(性) ，在这个过程中需要一个比平常更强的刺激。这两个不应期是由钠和钾离子通道分子状态的变化引起的。在动作电位后关闭时，钠通道进入“失活”状态，不管膜电位如何，钠通道都不能被打开ーー这就产生了绝对不应期(性)。即使有足够数量的钠离子通道已经过渡到它们的静息状态，也经常发生一小部分的钾离子通道仍然是开放的，这使得膜电位很难去极化，从而导致相对的不应期(性)。因为钾离子通道的密度和亚型在不同类型的神经元之间可能有很大的差异，相对的不应期(性)的持续时间是高度可变的。

The absolute refractory period is largely responsible for the unidirectional propagation of action potentials along axons.模板:Sfn At any given moment, the patch of axon behind the actively spiking part is refractory, but the patch in front, not having been activated recently, is capable of being stimulated by the depolarization from the action potential.

The absolute refractory period is largely responsible for the unidirectional propagation of action potentials along axons. At any given moment, the patch of axon behind the actively spiking part is refractory, but the patch in front, not having been activated recently, is capable of being stimulated by the depolarization from the action potential.

绝对不应期(性)主要负责沿轴突的动作电位的单向传播。在任何特定的时刻，活跃刺激部位后面的一小块轴突是不应激的，但是前面的一小块最近没有被激活，能够被动作电位的去极化刺激。

Propagation

Main article: Nerve conduction velocity

The action potential generated at the axon hillock propagates as a wave along the axon.模板:Sfn The currents flowing inwards at a point on the axon during an action potential spread out along the axon, and depolarize the adjacent sections of its membrane. If sufficiently strong, this depolarization provokes a similar action potential at the neighboring membrane patches. This basic mechanism was demonstrated by Alan Lloyd Hodgkin in 1937. After crushing or cooling nerve segments and thus blocking the action potentials, he showed that an action potential arriving on one side of the block could provoke another action potential on the other, provided that the blocked segment was sufficiently short.

The action potential generated at the axon hillock propagates as a wave along the axon. The currents flowing inwards at a point on the axon during an action potential spread out along the axon, and depolarize the adjacent sections of its membrane. If sufficiently strong, this depolarization provokes a similar action potential at the neighboring membrane patches. This basic mechanism was demonstrated by Alan Lloyd Hodgkin in 1937. After crushing or cooling nerve segments and thus blocking the action potentials, he showed that an action potential arriving on one side of the block could provoke another action potential on the other, provided that the blocked segment was sufficiently short.
*

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

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

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

一旦膜片上的一个动作电位发生了，膜片需要时间恢复才能再次激活。在分子水平上，这个绝对不应期(性)相当于电压激活的钠离子通道从失活状态恢复到闭合状态所需的时间。神经元中存在多种类型的电压激活钾通道。其中一些快速电流(a 型电流)失活，一些慢速失活或根本不失活; 这种变化保证了总有可用的复极电流来源，即使一些钾离子通道由于先前的去极化作用而失活。另一方面，在强去极化过程中，所有神经元电压激活钠通道在几毫秒内停止活动，从而使去极化不可能发生，直到相当一部分的钠通道恢复到它们的闭合状态。虽然它限制了放电的频率，但绝对不应期(性)电位确保了动作电位沿轴突只向一个方向移动。由于动作电位的作用，电流沿轴突向两个方向扩散。然而，只有轴突未激活的部分才能作出动作电位的反应; 刚刚激活的部分是没有反应的，直到动作电位安全地超出范围，不能再次激活该部分。在通常的正向传导中，动作电位从轴突柄向突触结节(轴突终端)传导，向相反方向传导的现象非常罕见。然而，如果一个实验室的轴突在它的中间被刺激，两半的轴突都是“新鲜的”，也就是说，没有被刺激，那么两个动作电位就会产生，一个朝向轴突小丘，另一个朝向突触结节。

Myelin and saltatory conduction

Main articles: Myelination and Saltatory conduction

In saltatory conduction, an action potential at one node of Ranvier causes inwards currents that depolarize the membrane at the next node, provoking a new action potential there; the action potential appears to "hop" from node to node.

In order to enable fast and efficient transduction of electrical signals in the nervous system, certain neuronal axons are covered with myelin sheaths. Myelin is a multilamellar membrane that enwraps the axon in segments separated by intervals known as nodes of Ranvier. It is produced by specialized cells: Schwann cells exclusively in the peripheral nervous system, and oligodendrocytes exclusively in the central nervous system. Myelin sheath reduces membrane capacitance and increases membrane resistance in the inter-node intervals, thus allowing a fast, saltatory movement of action potentials from node to node. Myelination is found mainly in vertebrates, but an analogous system has been discovered in a few invertebrates, such as some species of shrimp. Not all neurons in vertebrates are myelinated; for example, axons of the neurons comprising the autonomous nervous system are not, in general, myelinated.

In order to enable fast and efficient transduction of electrical signals in the nervous system, certain neuronal axons are covered with myelin sheaths. Myelin is a multilamellar membrane that enwraps the axon in segments separated by intervals known as nodes of Ranvier. It is produced by specialized cells: Schwann cells exclusively in the peripheral nervous system, and oligodendrocytes exclusively in the central nervous system. Myelin sheath reduces membrane capacitance and increases membrane resistance in the inter-node intervals, thus allowing a fast, saltatory movement of action potentials from node to node. Myelination is found mainly in vertebrates, but an analogous system has been discovered in a few invertebrates, such as some species of shrimp. Not all neurons in vertebrates are myelinated; for example, axons of the neurons comprising the autonomous nervous system are not, in general, myelinated.

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

Myelin prevents ions from entering or leaving the axon along myelinated segments. As a general rule, myelination increases the conduction velocity of action potentials and makes them more energy-efficient. Whether saltatory or not, the mean conduction velocity of an action potential ranges from 1 meter per second (m/s) to over 100 m/s, and, in general, increases with axonal diameter.

Myelin prevents ions from entering or leaving the axon along myelinated segments. As a general rule, myelination increases the conduction velocity of action potentials and makes them more energy-efficient. Whether saltatory or not, the mean conduction velocity of an action potential ranges from 1 meter per second (m/s) to over 100 m/s, and, in general, increases with axonal diameter.

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

Action potentials cannot propagate through the membrane in myelinated segments of the axon. However, the current is carried by the cytoplasm, which is sufficient to depolarize the first or second subsequent node of Ranvier. Instead, the ionic current from an action potential at one node of Ranvier provokes another action potential at the next node; this apparent "hopping" of the action potential from node to node is known as saltatory conduction. Although the mechanism of saltatory conduction was suggested in 1925 by Ralph Lillie, the first experimental evidence for saltatory conduction came from Ichiji Tasaki and Taiji Takeuchi and from Andrew Huxley and Robert Stämpfli. By contrast, in unmyelinated axons, the action potential provokes another in the membrane immediately adjacent, and moves continuously down the axon like a wave.

Action potentials cannot propagate through the membrane in myelinated segments of the axon. However, the current is carried by the cytoplasm, which is sufficient to depolarize the first or second subsequent node of Ranvier. Instead, the ionic current from an action potential at one node of Ranvier provokes another action potential at the next node; this apparent "hopping" of the action potential from node to node is known as saltatory conduction. Although the mechanism of saltatory conduction was suggested in 1925 by Ralph Lillie, See also the first experimental evidence for saltatory conduction came from Ichiji Tasaki and Taiji Takeuchi
* Tasaki, I in and from Andrew Huxley and Robert Stämpfli.
* By contrast, in unmyelinated axons, the action potential provokes another in the membrane immediately adjacent, and moves continuously down the axon like a wave.

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

Comparison of the conduction velocities of myelinated and unmyelinated axons in the cat.模板:Sfn The conduction velocity v of myelinated neurons varies roughly linearly with axon diameter d (that is, v ∝ d), whereas the speed of unmyelinated neurons varies roughly as the square root (v ∝模板:Radic). The red and blue curves are fits of experimental data, whereas the dotted lines are their theoretical extrapolations.

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. 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 selective advantage, since the human nervous system uses approximately 20% of the body's metabolic energy.

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. 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 selective advantage, since the human nervous system uses approximately 20% of the body's metabolic energy.

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

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

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

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

Some diseases degrade myelin and impair saltatory conduction, reducing the conduction velocity of action potentials. The most well-known of these is multiple sclerosis, in which the breakdown of myelin impairs coordinated movement.

Some diseases degrade myelin and impair saltatory conduction, reducing the conduction velocity of action potentials. The most well-known of these is multiple sclerosis, in which the breakdown of myelin impairs coordinated movement.Waxman, SG in

有些疾病会降低髓磷脂，损害跳跃式传导，降低动作电位的传导速度。其中最著名的是多发性硬化症，髓磷脂的分解妨碍了协调运动

Cable theory

Main article: Cable theory

Cable theory's simplified view of a neuronal fiber. The connected RC circuits correspond to adjacent segments of a passive neurite. The extracellular resistances r_e (the counterparts of the intracellular resistances r_i) are not shown, since they are usually negligibly small; the extracellular medium may be assumed to have the same voltage everywhere.

The flow of currents within an axon can be described quantitatively by cable theory and its elaborations, such as the compartmental model. Cable theory was developed in 1855 by Lord Kelvin to model the transatlantic telegraph cable and was shown to be relevant to neurons by Hodgkin and Rushton in 1946. In simple cable theory, the neuron is treated as an electrically passive, perfectly cylindrical transmission cable, which can be described by a partial differential equation

The flow of currents within an axon can be described quantitatively by cable theoryRall, W in and its elaborations, such as the compartmental model. Cable theory was developed in 1855 by Lord Kelvin to model the transatlantic telegraph cable and was shown to be relevant to neurons by Hodgkin and Rushton in 1946. In simple cable theory, the neuron is treated as an electrically passive, perfectly cylindrical transmission cable, which can be described by a partial differential equation

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

[math]\displaystyle{ \tau \frac{\partial V}{\partial t} = \lambda^2 \frac{\partial^2 V}{\partial x^2} - V }[/math]

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

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

where V(x, t) is the voltage across the membrane at a time t and a position x along the length of the neuron, and where λ and τ are the characteristic length and time scales on which those voltages decay in response to a stimulus. Referring to the circuit diagram on the right, these scales can be determined from the resistances and capacitances per unit length.模板:Sfn

where V(x, t) is the voltage across the membrane at a time t and a position x along the length of the neuron, and where λ and τ are the characteristic length and time scales on which those voltages decay in response to a stimulus. Referring to the circuit diagram on the right, these scales can be determined from the resistances and capacitances per unit length.

其中 v (x，t)是跨膜电压在时间 t 和位置 x 沿神经元长度，其中 λ 和 τ 是特征长度和时间尺度，这些电压衰减对刺激。参考右边的电路图，这些比例可以通过单位长度的电阻和电容来确定。

[math]\displaystyle{ \tau =\ r_m c_m \, }[/math]

\tau =\ r_m c_m \,

\tau =\ r_m c_m \,

[math]\displaystyle{ \lambda = \sqrt \frac{r_m}{r_\ell} }[/math]

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

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

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

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

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

= 终结 =

Chemical synapses

Main articles: Chemical synapse, Neurotransmitter, Excitatory postsynaptic potential, and Inhibitory postsynaptic potential

In general, action potentials that reach the synaptic knobs cause a neurotransmitter to be released into the synaptic cleft. Neurotransmitters are small molecules that may open ion channels in the postsynaptic cell; most axons have the same neurotransmitter at all of their termini. The arrival of the action potential opens voltage-sensitive calcium channels in the presynaptic membrane; the influx of calcium causes vesicles filled with neurotransmitter to migrate to the cell's surface and release their contents into the synaptic cleft. This complex process is inhibited by the neurotoxins tetanospasmin and botulinum toxin, which are responsible for tetanus and botulism, respectively.

In general, action potentials that reach the synaptic knobs cause a neurotransmitter to be released into the synaptic cleft. Neurotransmitters are small molecules that may open ion channels in the postsynaptic cell; most axons have the same neurotransmitter at all of their termini. The arrival of the action potential opens voltage-sensitive calcium channels in the presynaptic membrane; the influx of calcium causes vesicles filled with neurotransmitter to migrate to the cell's surface and release their contents into the synaptic cleft. This complex process is inhibited by the neurotoxins tetanospasmin and botulinum toxin, which are responsible for tetanus and botulism, respectively.

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

Electrical synapses between excitable cells allow ions to pass directly from one cell to another, and are much faster than chemical synapses.

Electrical synapses

Main articles: Electrical synapse, Gap junction, and Connexin

Some synapses dispense with the "middleman" of the neurotransmitter, and connect the presynaptic and postsynaptic cells together. When an action potential reaches such a synapse, the ionic currents flowing into the presynaptic cell can cross the barrier of the two cell membranes and enter the postsynaptic cell through pores known as connexons. Thus, the ionic currents of the presynaptic action potential can directly stimulate the postsynaptic cell. Electrical synapses allow for faster transmission because they do not require the slow diffusion of neurotransmitters across the synaptic cleft. Hence, electrical synapses are used whenever fast response and coordination of timing are crucial, as in escape reflexes, the retina of vertebrates, and the heart.

Some synapses dispense with the "middleman" of the neurotransmitter, and connect the presynaptic and postsynaptic cells together. When an action potential reaches such a synapse, the ionic currents flowing into the presynaptic cell can cross the barrier of the two cell membranes and enter the postsynaptic cell through pores known as connexons. Thus, the ionic currents of the presynaptic action potential can directly stimulate the postsynaptic cell. Electrical synapses allow for faster transmission because they do not require the slow diffusion of neurotransmitters across the synaptic cleft. Hence, electrical synapses are used whenever fast response and coordination of timing are crucial, as in escape reflexes, the retina of vertebrates, and the heart.

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

Neuromuscular junctions

Main articles: Neuromuscular junction, Acetylcholine receptor, and Cholinesterase enzyme

A special case of a chemical synapse is the neuromuscular junction, in which the axon of a motor neuron terminates on a muscle fiber. In such cases, the released neurotransmitter is acetylcholine, which binds to the acetylcholine receptor, an integral membrane protein in the membrane (the sarcolemma) of the muscle fiber. However, the acetylcholine does not remain bound; rather, it dissociates and is hydrolyzed by the enzyme, acetylcholinesterase, located in the synapse. This enzyme quickly reduces the stimulus to the muscle, which allows the degree and timing of muscular contraction to be regulated delicately. Some poisons inactivate acetylcholinesterase to prevent this control, such as the nerve agents sarin and tabun, and the insecticides diazinon and malathion.

A special case of a chemical synapse is the neuromuscular junction, in which the axon of a motor neuron terminates on a muscle fiber. In such cases, the released neurotransmitter is acetylcholine, which binds to the acetylcholine receptor, an integral membrane protein in the membrane (the sarcolemma) of the muscle fiber. However, the acetylcholine does not remain bound; rather, it dissociates and is hydrolyzed by the enzyme, acetylcholinesterase, located in the synapse. This enzyme quickly reduces the stimulus to the muscle, which allows the degree and timing of muscular contraction to be regulated delicately. Some poisons inactivate acetylcholinesterase to prevent this control, such as the nerve agents sarin and tabun, and the insecticides diazinon and malathion.

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

= = 其他细胞类型 =

Cardiac action potentials

Main articles: Cardiac action potential, Electrical conduction system of the heart, Cardiac pacemaker, and Heart arrhythmia

生成缩略图出错：convert-im6.q16: non-conforming drawing primitive definition `font-style' @ error/draw.c/RenderMVGContent/4404.

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.

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. 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. 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.

心脏动作电位与神经元动作电位的不同之处在于，心脏动作电位有一个延长的平台期，在这个平台期间，膜在被钾电流重新极化之前以高电压保持几百毫秒。这个平台是由于慢速钙通道开放的作用，即使在钠通道失去活性之后，仍然保持膜电位接近其平衡电位。

The cardiac action potential plays an important role in coordinating the contraction of the heart. The cardiac cells of the sinoatrial node provide the pacemaker potential that synchronizes the heart. The action potentials of those cells propagate to and through the atrioventricular node (AV node), which is normally the only conduction pathway between the atria and the ventricles. Action potentials from the AV node travel through the bundle of His and thence to the Purkinje fibers. Conversely, anomalies in the cardiac action potential—whether due to a congenital mutation or injury—can lead to human pathologies, especially arrhythmias. Several anti-arrhythmia drugs act on the cardiac action potential, such as quinidine, lidocaine, beta blockers, and verapamil.

The cardiac action potential plays an important role in coordinating the contraction of the heart. The cardiac cells of the sinoatrial node provide the pacemaker potential that synchronizes the heart. The action potentials of those cells propagate to and through the atrioventricular node (AV node), which is normally the only conduction pathway between the atria and the ventricles. Action potentials from the AV node travel through the bundle of His and thence to the Purkinje fibers.Note that these Purkinje fibers are muscle fibers and not related to the Purkinje cells, which are neurons found in the cerebellum. Conversely, anomalies in the cardiac action potential—whether due to a congenital mutation or injury—can lead to human pathologies, especially arrhythmias. Several anti-arrhythmia drugs act on the cardiac action potential, such as quinidine, lidocaine, beta blockers, and verapamil.

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

Muscular action potentials

Main articles: Neuromuscular junction and Muscle contraction

The action potential in a normal skeletal muscle cell is similar to the action potential in neurons.模板:Sfn Action potentials result from the depolarization of the cell membrane (the sarcolemma), which opens voltage-sensitive sodium channels; these become inactivated and the membrane is repolarized through the outward current of potassium ions. The resting potential prior to the action potential is typically −90mV, somewhat more negative than typical neurons. The muscle action potential lasts roughly 2–4 ms, the absolute refractory period is roughly 1–3 ms, and the conduction velocity along the muscle is roughly 5 m/s. The action potential releases calcium ions that free up the tropomyosin and allow the muscle to contract. Muscle action potentials are provoked by the arrival of a pre-synaptic neuronal action potential at the neuromuscular junction, which is a common target for neurotoxins.

The action potential in a normal skeletal muscle cell is similar to the action potential in neurons. Action potentials result from the depolarization of the cell membrane (the sarcolemma), which opens voltage-sensitive sodium channels; these become inactivated and the membrane is repolarized through the outward current of potassium ions. The resting potential prior to the action potential is typically −90mV, somewhat more negative than typical neurons. The muscle action potential lasts roughly 2–4 ms, the absolute refractory period is roughly 1–3 ms, and the conduction velocity along the muscle is roughly 5 m/s. The action potential releases calcium ions that free up the tropomyosin and allow the muscle to contract. Muscle action potentials are provoked by the arrival of a pre-synaptic neuronal action potential at the neuromuscular junction, which is a common target for neurotoxins.

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

Plant action potentials

See also: Variation potential

Plant and fungal cells are also electrically excitable. The fundamental difference from animal action potentials is that the depolarization in plant cells is not accomplished by an uptake of positive sodium ions, but by release of negative chloride ions. In 1906, J. C. Bose published the first measurements of action potentials in plants, which had previously been discovered by Burdon-Sanderson and Darwin. An increase in cytoplasmic calcium ions may be the cause of anion release into the cell. This makes calcium a precursor to ion movements, such as the influx of negative chloride ions and efflux of positive potassium ions, as seen in barley leaves.

Plant and fungal cells are also electrically excitable. The fundamental difference from animal action potentials is that the depolarization in plant cells is not accomplished by an uptake of positive sodium ions, but by release of negative chloride ions. In 1906, J. C. Bose published the first measurements of action potentials in plants, which had previously been discovered by Burdon-Sanderson and Darwin. An increase in cytoplasmic calcium ions may be the cause of anion release into the cell. This makes calcium a precursor to ion movements, such as the influx of negative chloride ions and efflux of positive potassium ions, as seen in barley leaves.

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

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

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

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

Some plants (e.g. Dionaea muscipula) use sodium-gated channels to operate movements and essentially "count". Dionaea muscipula, also known as the Venus flytrap, is found in subtropical wetlands in North and South Carolina. When there are poor soil nutrients, the flytrap relies on a diet of insects and animals. Despite research on the plant, there lacks an understanding behind the molecular basis to the Venus flytraps, and carnivore plants in general.

Some plants (e.g. Dionaea muscipula) use sodium-gated channels to operate movements and essentially "count". Dionaea muscipula, also known as the Venus flytrap, is found in subtropical wetlands in North and South Carolina. When there are poor soil nutrients, the flytrap relies on a diet of insects and animals. Despite research on the plant, there lacks an understanding behind the molecular basis to the Venus flytraps, and carnivore plants in general.

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

However, plenty of research has been done on action potentials and how they affect movement and clockwork within the Venus flytrap. To start, the resting membrane potential of the Venus flytrap (-120mV) is lower than animal cells (usually -90mV to -40mV). The lower resting potential makes it easier to activate an action potential. Thus, when an insect lands on the trap of the plant, it triggers a hair-like mechanoreceptor. This receptor then activates an action potential which lasts around 1.5 ms. Ultimately, this causes an increase of positive Calcium ions into the cell, slightly depolarizing it.

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

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

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

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

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

Together with the subsequent release of positive potassium ions the action potential in plants involves an osmotic loss of salt (KCl). Whereas, the animal action potential is osmotically neutral because equal amounts of entering sodium and leaving potassium cancel each other osmotically. The interaction of electrical and osmotic relations in plant cells appears to have arisen from an osmotic function of electrical excitability in a common unicellular ancestors of plants and animals under changing salinity conditions. Further, the present function of rapid signal transmission is seen as a newer accomplishment of metazoan cells in a more stable osmotic environment. It is likely that the familiar signaling function of action potentials in some vascular plants (e.g. Mimosa pudica) arose independently from that in metazoan excitable cells.

Together with the subsequent release of positive potassium ions the action potential in plants involves an osmotic loss of salt (KCl). Whereas, the animal action potential is osmotically neutral because equal amounts of entering sodium and leaving potassium cancel each other osmotically. The interaction of electrical and osmotic relations in plant cells appears to have arisen from an osmotic function of electrical excitability in a common unicellular ancestors of plants and animals under changing salinity conditions. Further, the present function of rapid signal transmission is seen as a newer accomplishment of metazoan cells in a more stable osmotic environment. Gradmann, D; Mummert, H in It is likely that the familiar signaling function of action potentials in some vascular plants (e.g. Mimosa pudica) arose independently from that in metazoan excitable cells.

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

Unlike the rising phase and peak, the falling phase and after-hyperpolarization seem to depend primarily on cations that are not calcium. To initiate repolarization, the cell requires movement of potassium out of the cell through passive transportation on the membrane. This differs from neurons because the movement of potassium does not dominate the decrease in membrane potential; In fact, to fully repolarize, a plant cell requires energy in the form of ATP to assist in the release of hydrogen from the cell – utilizing a transporter commonly known as H+-ATPase.

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

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

Taxonomic distribution and evolutionary advantages

Action potentials are found throughout multicellular organisms, including plants, invertebrates such as insects, and vertebrates such as reptiles and mammals. Sponges seem to be the main phylum of multicellular eukaryotes that does not transmit action potentials, although some studies have suggested that these organisms have a form of electrical signaling, too. The resting potential, as well as the size and duration of the action potential, have not varied much with evolution, although the conduction velocity does vary dramatically with axonal diameter and myelination.

Action potentials are found throughout multicellular organisms, including plants, invertebrates such as insects, and vertebrates such as reptiles and mammals. Sponges seem to be the main phylum of multicellular eukaryotes that does not transmit action potentials, although some studies have suggested that these organisms have a form of electrical signaling, too. The resting potential, as well as the size and duration of the action potential, have not varied much with evolution, although the conduction velocity does vary dramatically with axonal diameter and myelination.

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

Comparison of action potentials (APs) from a representative cross-section of animals模板:Sfn

Animal	Cell type	Resting potential (mV)	AP increase (mV)	AP duration (ms)	Conduction speed (m/s)
Squid (Loligo)	Giant axon	−60	120	0.75	35
Earthworm (Lumbricus)	Median giant fiber	−70	100	1.0	30
Cockroach (Periplaneta)	Giant fiber	−70	80–104	0.4	10
Frog (Rana)	Sciatic nerve axon	−60 to −80	110–130	1.0	7–30
Cat (Felis)	Spinal motor neuron	−55 to −80	80–110	1–1.5	30–120

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

Animal	Cell type	Resting potential (mV)	AP increase (mV)	AP duration (ms)	Conduction speed (m/s)
Squid (Loligo)	Giant axon	−60	120	0.75	35
Earthworm (Lumbricus)	Median giant fiber	−70	100	1.0	30
Cockroach (Periplaneta)	Giant fiber	−70	80–104	0.4	10
Frog (Rana)	Sciatic nerve axon	−60 to −80	110–130	1.0	7–30
Cat (Felis)	Spinal motor neuron	−55 to −80	80–110	1–1.5	30–120

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

动物! ！手机类型! ！Resting potential (mV)	-	巨轴突 | 60美元120美元0.75 | 35美元 | -	中间巨纤维 | | 70美元100美元1.0 | 30 | -	| 巨型纤维 | | 70美元80-1040.4 | | 10 | -	坐骨神经轴突 | 60到80110-1301.0 | 7-30-	脊髓运动神经元 | 55到8080-1101-1.5 | 30-120 | } Given its conservation throughout evolution, the action potential seems to confer evolutionary advantages. One function of action potentials is rapid, long-range signaling within the organism; the conduction velocity can exceed 110 m/s, which is one-third the speed of sound. For comparison, a hormone molecule carried in the bloodstream moves at roughly 8 m/s in large arteries. Part of this function is the tight coordination of mechanical events, such as the contraction of the heart. A second function is the computation associated with its generation. Being an all-or-none signal that does not decay with transmission distance, the action potential has similar advantages to digital electronics. The integration of various dendritic signals at the axon hillock and its thresholding to form a complex train of action potentials is another form of computation, one that has been exploited biologically to form central pattern generators and mimicked in artificial neural networks. Given its conservation throughout evolution, the action potential seems to confer evolutionary advantages. One function of action potentials is rapid, long-range signaling within the organism; the conduction velocity can exceed 110 m/s, which is one-third the speed of sound. For comparison, a hormone molecule carried in the bloodstream moves at roughly 8 m/s in large arteries. Part of this function is the tight coordination of mechanical events, such as the contraction of the heart. A second function is the computation associated with its generation. Being an all-or-none signal that does not decay with transmission distance, the action potential has similar advantages to digital electronics. The integration of various dendritic signals at the axon hillock and its thresholding to form a complex train of action potentials is another form of computation, one that has been exploited biologically to form central pattern generators and mimicked in artificial neural networks. 鉴于动作电位在整个进化过程中的保守性，它似乎赋予了进化优势。动作电位的一个功能是在生物体内快速的远程信号传导，传导速度可以超过110米/秒，这是声速的三分之一。相比之下，血液中携带的荷尔蒙分子在大动脉中的运动速度大约为每秒8米。这个功能的一部分是机械事件的紧密协调，例如心脏的收缩。第二个函数是与其生成相关的计算。动作电位作为一种全或无信号，不随传输距离衰减，与数字电子技术具有相似的优点。轴突小丘上各种树突信号的整合及其阈值化形成一系列复杂的动作电位是另一种形式的计算方法，这种方法已被生物学方法用来形成中心模式发生器，并在人工神经网络中进行模拟。 The common prokaryotic/eukaryotic ancestor, which lived perhaps four billion years ago, is believed to have had voltage-gated channels. This functionality was likely, at some later point, cross-purposed to provide a communication mechanism. Even modern single-celled bacteria can utilize action potentials to communicate with other bacteria in the same biofilm. The common prokaryotic/eukaryotic ancestor, which lived perhaps four billion years ago, is believed to have had voltage-gated channels. This functionality was likely, at some later point, cross-purposed to provide a communication mechanism. Even modern single-celled bacteria can utilize action potentials to communicate with other bacteria in the same biofilm. 生活在大约40亿年前的原核/真核生物的共同祖先，被认为具有电压门控通道。在以后的某个时候，这个功能可能会被用来提供一个通信机制。即使是现代的单细胞细菌也可以利用动作电位与生物膜中的其他细菌进行交流。 Experimental methods See also: Electrophysiology Giant axons of the longfin inshore squid (Doryteuthis pealeii) were crucial for scientists to understand the action potential. 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 electrodes 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 electrodes enough that the voltage inside a single cell could be recorded. 动作电位的研究需要开发新的实验方法。在1955年之前，最初的工作主要是由艾伦·劳埃德·霍奇金和 Andrew Fielding Huxley 完成的，他们因为在描述神经传导的离子基础方面做出的贡献，和约翰·卡鲁·埃克尔斯一起被授予1963年诺贝尔生理学或医学奖。它着重于三个目标: 从单个神经元或轴突中分离出信号，发展快速、灵敏的电子设备，以及缩小电极，使单个细胞内的电压能够被记录下来。 The first problem was solved by studying the giant axons found in the neurons of the squid (Loligo forbesii and Doryteuthis pealeii, at the time classified as Loligo pealeii). These axons are so large in diameter (roughly 1 mm, or 100-fold larger than a typical neuron) that they can be seen with the naked eye, making them easy to extract and manipulate. However, they are not representative of all excitable cells, and numerous other systems with action potentials have been studied. The first problem was solved by studying the giant axons found in the neurons of the squid (Loligo forbesii and Doryteuthis pealeii, at the time classified as Loligo pealeii). These axons are so large in diameter (roughly 1 mm, or 100-fold larger than a typical neuron) that they can be seen with the naked eye, making them easy to extract and manipulate. However, they are not representative of all excitable cells, and numerous other systems with action potentials have been studied. 第一个问题通过研究乌贼神经元中发现的巨大轴突(Loligo forbesii 和 Doryteuthis pealeii，当时被归类为 Loligo pealeii)得到了解决。这些轴突直径很大(大约1毫米，比一个典型的神经元大100倍) ，可以用肉眼看到，因此很容易提取和操作。然而，它们并不代表所有可兴奋细胞，许多其他具有动作电位的系统已被研究。 The second problem was addressed with the crucial development of the voltage clamp, which permitted experimenters to study the ionic currents underlying an action potential in isolation, and eliminated a key source of electronic noise, the current IC associated with the capacitance C of the membrane.模板:Sfn Since the current equals C times the rate of change of the transmembrane voltage Vm, the solution was to design a circuit that kept Vm fixed (zero rate of change) regardless of the currents flowing across the membrane. Thus, the current required to keep Vm at a fixed value is a direct reflection of the current flowing through the membrane. Other electronic advances included the use of Faraday cages and electronics with high input impedance, so that the measurement itself did not affect the voltage being measured.模板:Sfn The second problem was addressed with the crucial development of the voltage clamp, which permitted experimenters to study the ionic currents underlying an action potential in isolation, and eliminated a key source of electronic noise, the current IC associated with the capacitance C of the membrane. Since the current equals C times the rate of change of the transmembrane voltage Vm, the solution was to design a circuit that kept Vm fixed (zero rate of change) regardless of the currents flowing across the membrane. Thus, the current required to keep Vm at a fixed value is a direct reflection of the current flowing through the membrane. Other electronic advances included the use of Faraday cages and electronics with high input impedance, so that the measurement itself did not affect the voltage being measured. 第二个问题是关于电压钳的关键发展，它允许实验者在隔离的情况下研究作用于动作电位的离子电流，并消除了电子噪声的一个关键来源---- 与膜电容 c 相关的电流 IC。由于电流等于 c 乘以跨膜电压 Vm 的变化率，所以解决方案是设计一个电路，使 Vm 保持固定(零变化率) ，而不管跨膜电流的变化。因此，使 Vm 保持在一个固定值所需的电流是流过薄膜的电流的直接反射。其他电子方面的进步包括使用法拉第笼和具有高输入阻抗的电子器件，这样测量本身就不会影响被测量的电压。 The third problem, that of obtaining electrodes small enough to record voltages within a single axon without perturbing it, was solved in 1949 with the invention of the glass micropipette electrode, which was quickly adopted by other researchers. Refinements of this method are able to produce electrode tips that are as fine as 100 Å (10 nm), which also confers high input impedance. Action potentials may also be recorded with small metal electrodes placed just next to a neuron, with neurochips containing EOSFETs, or optically with dyes that are sensitive to Ca2+ or to voltage. The third problem, that of obtaining electrodes small enough to record voltages within a single axon without perturbing it, was solved in 1949 with the invention of the glass micropipette electrode, which was quickly adopted by other researchers. Refinements of this method are able to produce electrode tips that are as fine as 100 Å (10 nm), which also confers high input impedance.Snell, FM in Action potentials may also be recorded with small metal electrodes placed just next to a neuron, with neurochips containing EOSFETs, or optically with dyes that are sensitive to Ca2+ or to voltage. * 第三个问题是如何获得足够小的电极来记录单个轴突内的电压而不对其造成干扰，这个问题在1949年由于玻璃微移液管电极的发明而得到解决，并且很快被其他研究人员采用。这种方法的改进可以生产出100纳米的电极尖端，同时也提供了高的输入阻抗。动作电位中的 Snell 和 FM 也可以用放置在神经元旁的小金属电极记录下来，用含有 eosfet 的神经芯片，或者用对 Ca < sup > 2 + 或电压敏感的染料记录下来。< br/> * As revealed by a patch clamp electrode, an ion channel has two states: open (high conductance) and closed (low conductance). While glass micropipette electrodes measure the sum of the currents passing through many ion channels, studying the electrical properties of a single ion channel became possible in the 1970s with the development of the patch clamp by Erwin Neher and Bert Sakmann. For this discovery, they were awarded the Nobel Prize in Physiology or Medicine in 1991. Patch-clamping verified that ionic channels have discrete states of conductance, such as open, closed and inactivated. While glass micropipette electrodes measure the sum of the currents passing through many ion channels, studying the electrical properties of a single ion channel became possible in the 1970s with the development of the patch clamp by Erwin Neher and Bert Sakmann. For this discovery, they were awarded the Nobel Prize in Physiology or Medicine in 1991. Patch-clamping verified that ionic channels have discrete states of conductance, such as open, closed and inactivated. 玻璃微吸管电极测量通过许多离子通道的电流总和，研究单个离子通道的电学性质在20世纪70年代埃尔温 · 内尔和伯特 · 萨克曼发明的膜片钳成为可能。由于这一发现，他们在1991年被授予诺贝尔生理学或医学奖科学奖。膜片钳技术证实了离子通道具有分立的电导状态，如开放状态、闭合状态和失活状态。 Optical imaging technologies have been developed in recent years to measure action potentials, either via simultaneous multisite recordings or with ultra-spatial resolution. Using voltage-sensitive dyes, action potentials have been optically recorded from a tiny patch of cardiomyocyte membrane. Optical imaging technologies have been developed in recent years to measure action potentials, either via simultaneous multisite recordings or with ultra-spatial resolution. Using voltage-sensitive dyes, action potentials have been optically recorded from a tiny patch of cardiomyocyte membrane. 近年来发展了光学成像技术，通过同时多点记录或超空间分辨率来测量动作电位。利用电压敏感染料，从一小块心肌细胞膜上记录了动作电位。 Neurotoxins Tetrodotoxin is a lethal toxin found in pufferfish that inhibits the voltage-sensitive sodium channel, halting action potentials. Several neurotoxins, both natural and synthetic, are designed to block the action potential. Tetrodotoxin from the pufferfish and saxitoxin from the Gonyaulax (the dinoflagellate genus responsible for "red tides") block action potentials by inhibiting the voltage-sensitive sodium channel; similarly, dendrotoxin from the black mamba snake inhibits the voltage-sensitive potassium channel. Such inhibitors of ion channels serve an important research purpose, by allowing scientists to "turn off" specific channels at will, thus isolating the other channels' contributions; they can also be useful in purifying ion channels by affinity chromatography or in assaying their concentration. However, such inhibitors also make effective neurotoxins, and have been considered for use as chemical weapons. Neurotoxins aimed at the ion channels of insects have been effective insecticides; one example is the synthetic permethrin, which prolongs the activation of the sodium channels involved in action potentials. The ion channels of insects are sufficiently different from their human counterparts that there are few side effects in humans. Several neurotoxins, both natural and synthetic, are designed to block the action potential. Tetrodotoxin from the pufferfish and saxitoxin from the Gonyaulax (the dinoflagellate genus responsible for "red tides") block action potentials by inhibiting the voltage-sensitive sodium channel; * * similarly, dendrotoxin from the black mamba snake inhibits the voltage-sensitive potassium channel. Such inhibitors of ion channels serve an important research purpose, by allowing scientists to "turn off" specific channels at will, thus isolating the other channels' contributions; they can also be useful in purifying ion channels by affinity chromatography or in assaying their concentration. However, such inhibitors also make effective neurotoxins, and have been considered for use as chemical weapons. Neurotoxins aimed at the ion channels of insects have been effective insecticides; one example is the synthetic permethrin, which prolongs the activation of the sodium channels involved in action potentials. The ion channels of insects are sufficiently different from their human counterparts that there are few side effects in humans. 一些天然和人工的神经毒素被设计用来阻断动作电位。来自河豚的河豚毒素和来自沟鞭藻属的石房蛤毒素通过抑制电压敏感性钠通道来阻断动作电位; 同样地，黑曼巴蛇的树眼镜蛇毒素也会抑制电压敏感性钾离子通道。这种离子通道的抑制剂有一个重要的研究目的，它可以让科学家随意关闭特定的通道，从而分离出其他通道的贡献; 它们也可以用亲和色谱法来净化离子通道或测定它们的浓度。然而，这些抑制剂也能产生有效的神经毒素，并被认为是化学武器。针对昆虫离子通道的神经毒素一直是有效的杀虫剂，其中一个例子是合成氯菊酯，它延长了与动作电位有关的钠通道的激活。昆虫的离子通道与人类的离子通道完全不同，因此对人类几乎没有副作用。 History Image of two Purkinje cells (labeled as A) drawn by Santiago Ramón y Cajal in 1899. Large trees of dendrites feed into the soma, from which a single axon emerges and moves generally downwards with a few branch points. The smaller cells labeled B are granule cells. The role of electricity in the nervous systems of animals was first observed in dissected frogs by Luigi Galvani, who studied it from 1791 to 1797. Galvani's results stimulated Alessandro Volta to develop the Voltaic pile—the earliest-known electric battery—with which he studied animal electricity (such as electric eels) and the physiological responses to applied direct-current voltages. The role of electricity in the nervous systems of animals was first observed in dissected frogs by Luigi Galvani, who studied it from 1791 to 1797. Galvani's results stimulated Alessandro Volta to develop the Voltaic pile—the earliest-known electric battery—with which he studied animal electricity (such as electric eels) and the physiological responses to applied direct-current voltages. 电在动物神经系统中的作用最早是由路易吉 · 伽伐尼在解剖的青蛙中观察到的，他从1791年到1797年研究了这一现象。伽伐尼的研究结果激发了亚历山德罗·伏特发明了伏打电堆ーー已知最早的电池ーー他用这种电池研究了动物电(如电鳗)以及对直流电压的生理反应。 Scientists of the 19th century studied the propagation of electrical signals in whole nerves (i.e., bundles of neurons) and demonstrated that nervous tissue was made up of cells, instead of an interconnected network of tubes (a reticulum).模板:Sfnm Carlo Matteucci followed up Galvani's studies and demonstrated that cell membranes had a voltage across them and could produce direct current. Matteucci's work inspired the German physiologist, Emil du Bois-Reymond, who discovered the action potential in 1843. The conduction velocity of action potentials was first measured in 1850 by du Bois-Reymond's friend, Hermann von Helmholtz. To establish that nervous tissue is made up of discrete cells, the Spanish physician Santiago Ramón y Cajal and his students used a stain developed by Camillo Golgi to reveal the myriad shapes of neurons, which they rendered painstakingly. For their discoveries, Golgi and Ramón y Cajal were awarded the 1906 Nobel Prize in Physiology. Their work resolved a long-standing controversy in the neuroanatomy of the 19th century; Golgi himself had argued for the network model of the nervous system. Scientists of the 19th century studied the propagation of electrical signals in whole nerves (i.e., bundles of neurons) and demonstrated that nervous tissue was made up of cells, instead of an interconnected network of tubes (a reticulum). Carlo Matteucci followed up Galvani's studies and demonstrated that cell membranes had a voltage across them and could produce direct current. Matteucci's work inspired the German physiologist, Emil du Bois-Reymond, who discovered the action potential in 1843. The conduction velocity of action potentials was first measured in 1850 by du Bois-Reymond's friend, Hermann von Helmholtz.Olesko, Kathryn M., and Frederic L. Holmes. "Experiment, Quantification and Discovery: Helmholtz's Early Physiological Researches, 1843-50". In Hermann von Helmholtz and the Foundations of Nineteenth Century Science, ed. David Cahan, 50-108. Berkeley; Los Angeles; London: University of California, 1994. To establish that nervous tissue is made up of discrete cells, the Spanish physician Santiago Ramón y Cajal and his students used a stain developed by Camillo Golgi to reveal the myriad shapes of neurons, which they rendered painstakingly. For their discoveries, Golgi and Ramón y Cajal were awarded the 1906 Nobel Prize in Physiology. Their work resolved a long-standing controversy in the neuroanatomy of the 19th century; Golgi himself had argued for the network model of the nervous system. 19世纪的科学家研究了电信号在整个神经(即神经元束)中的传播，并证明神经组织是由细胞组成的，而不是一个互相连接的管网(网状结构)。卡洛 · 马特乌奇继续伽伐尼的研究，证明细胞膜上有一个电压，可以产生直流电。马特乌奇的工作启发了德国生理学家埃米尔 · 杜 · 布瓦-雷蒙德，后者在1843年发现了动作电位。动作电位的传导速度最早是在1850年由杜波依斯-雷蒙德的朋友赫尔曼·冯·亥姆霍兹 · 雷蒙德测量的。凯瑟琳 · m · 奥列斯科和弗雷德里克 · l · 福尔摩斯。“实验、量化与发现: 亥姆霍兹早期生理学研究，1843-50”。在《赫尔曼·冯·亥姆霍兹和19世纪科学的基础》 ，ed。大卫 · 卡汉，50-108。伯克利; 洛杉矶; 伦敦: 加州大学，1994年。为了证明神经组织是由离散的细胞组成的，西班牙物理学家圣地亚哥·拉蒙-卡哈尔和他的学生们使用了 Camillo Golgi 开发的染色剂来显示神经元的无数形状，他们煞费苦心地进行了渲染。由于他们的发现，高尔基和拉蒙 · 卡哈尔获得了1906年的诺贝尔生理学奖。他们的工作解决了19世纪神经解剖学中长期存在的争议; 高尔基自己则主张神经系统的网络模型。 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. 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 permeability of the axonal membrane to ions.模板:Sfn Bernstein's hypothesis was confirmed by Ken Cole and Howard Curtis, who showed that membrane conductance increases during an action potential. In 1907, Louis Lapicque suggested that the action potential was generated as a threshold was crossed, what would be later shown as a product of the dynamical systems of ionic conductances. In 1949, 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. They made the first actual recording of the electrical changes across the neuronal membrane that mediate the action potential. 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. Hodgkin and Huxley correlated the properties of their mathematical model with discrete ion channels 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 clamping to examine the conductance states of individual ion channels. 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, through the atomic-resolution crystal structures, fluorescence distance measurements and cryo-electron microscopy studies. 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 permeability of the axonal membrane to ions. Bernstein's hypothesis was confirmed by Ken Cole and Howard Curtis, who showed that membrane conductance increases during an action potential. In 1907, Louis Lapicque suggested that the action potential was generated as a threshold was crossed, what would be later shown as a product of the dynamical systems of ionic conductances. In 1949, 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. They made the first actual recording of the electrical changes across the neuronal membrane that mediate the action potential. 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. * * * * Hodgkin and Huxley correlated the properties of their mathematical model with discrete ion channels 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 clamping to examine the conductance states of individual ion channels. * * 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, through the atomic-resolution crystal structures, * * fluorescence distance measurements * * and cryo-electron microscopy studies. * 20世纪是20世纪电生理学的重要时期。1902年和1912年，朱利叶斯 · 伯恩斯坦提出了动作电位是由轴突膜对离子的渗透性改变引起的假说。肯 · 科尔和霍华德 · 柯蒂斯证实了伯恩斯坦的假设，他们发现在动作电位期间膜电导增加。1907年，路易斯 · 拉皮克提出，动作电位产生的阈值被跨越，后来被证明为离子电导动力学系统的乘积。1949年，Alan Hodgkin 和 Bernard Katz 提出了 Bernstein 的假说，他们认为轴突膜对不同的离子可能有不同的通透性; 特别是，他们证明了钠通透性对动作电位的关键作用。他们首次实际记录了神经元膜上的电变化，这些电变化介导了动作电位。这一系列的研究在 Hodgkin，Katz 和 Andrew Huxley 的5篇1952年的论文中达到了顶峰，他们应用电压钳技术来确定轴突膜对钠离子和钾离子的通透性对电压和时间的依赖性，从而能够定量地重建动作电位。< br/> < br/> < br/> < br/> < br/> < Hodgkin 和 Huxley 将其数学模型的性质与离散离子通道相关联，离散离子通道可以存在于几种不同的状态，包括“开放”、“封闭”和“失活”。他们的假设在20世纪70年代中期和80年代得到 Erwin Neher 和 Bert Sakmann 的证实，他们发明了膜片钳技术来检测单个离子通道的电导状态。在21世纪，通过原子分辨率晶体结构，研究人员开始了解这些电导态的结构基础，以及离子种类的通道选择性，荧光距离测量 < br/> < br/> 和冷冻电子显微研究。< br/> * Julius Bernstein was also the first to introduce the Nernst equation for resting potential across the membrane; this was generalized by David E. Goldman to the eponymous Goldman equation in 1943. The sodium–potassium pump was identified in 1957 and its properties gradually elucidated, culminating in the determination of its atomic-resolution structure by X-ray crystallography. The crystal structures of related ionic pumps have also been solved, giving a broader view of how these molecular machines work. Julius Bernstein was also the first to introduce the Nernst equation for resting potential across the membrane; this was generalized by David E. Goldman to the eponymous Goldman equation in 1943. The sodium–potassium pump was identified in 1957 and its properties gradually elucidated, culminating in the determination of its atomic-resolution structure by X-ray crystallography. The crystal structures of related ionic pumps have also been solved, giving a broader view of how these molecular machines work. 也是第一个将静息电位的能斯特方程引入到薄膜上的人; David e. Goldman 在1943年将这个方程推广到了以他的名字命名的戈德曼方程。钠钾泵在1957年被鉴定出来，它的性质逐渐被阐明，最终由 X光散射技术测定了它的原子分辨率结构。相关的离子泵的晶体结构也已经被解决，从而为这些分子机器如何工作提供了更广阔的视野。 Quantitative models Main article: Quantitative models of the action potential Equivalent electrical circuit for the Hodgkin–Huxley model of the action potential. Im and Vm represent the current through, and the voltage across, a small patch of membrane, respectively. The Cm represents the capacitance of the membrane patch, whereas the four g's represent the 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-sensitive ion channels. The two conductances on the right help determine the resting membrane potential. 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 equations (ODEs). Although the Hodgkin–Huxley model may be a simplification with few limitations compared to the realistic nervous membrane as it exists in nature, its complexity has inspired several even-more-simplified models,模板:Sfn such as the Morris–Lecar model and the FitzHugh–Nagumo model, 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, have been well-studied within mathematics, computation and electronics. 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. 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模板:Sfnm and simple reflexes, such as escape reflexes and others controlled by central pattern generators. 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 equations (ODEs). Although the Hodgkin–Huxley model may be a simplification with few limitations compared to the realistic nervous membrane as it exists in nature, its complexity has inspired several even-more-simplified models,* * such as the Morris–Lecar model and the FitzHugh–Nagumo model, * 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, * * * * have been well-studied within mathematics,Sato, S; Fukai, H; Nomura, T; Doi, S in * FitzHugh, R in * * computationNelson, ME; Rinzel, J in * Rinzel, J & Ermentrout, GB; in and electronics. 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. 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 and simple reflexes, such as escape reflexes and others controlled by central pattern generators.Getting, PA in 数学模型和计算模型对于理解动作电位是必不可少的，它们提供的预测可以通过实验数据进行检验，从而为理论提供严格的检验。早期神经模型中最重要和最准确的是 Hodgkin-Huxley 模型，它通过一组四个常微分方程(ODEs)来描述动作电位。虽然 Hodgkin-Huxley 模型可能是一个简化的模型，但与实际存在的神经膜相比，它的局限性很小，其复杂性激发了几个更简化的模型，* < br/> * ，例如 Morris-Lecar 模型和 FitzHugh-Nagumo 模型，< br/> * 这两个模型都只有两个耦合的常微分方程。Hodgkin-Huxley 模型和 FitzHugh-Nagumo 模型以及它们的近亲，如 Bonhoeffer-Van der Pol 模型，< br/> * < br/> * < br/> * < br/> * < br/> * < br/> * < br/> * < br/> * 已经在数学中得到了很好的研究，Sato，s; Fukai，h; Nomura，t; Doi，s in < br/> * FitzHugh，r in < br/> * < br/> * computationNelson，ME; Rinzel，j in </> * Rinzel，j & ertrout，GB; in electronics;。然而，简单的生成电位和动作电位模型并不能准确地再现近阈值神经元刺激速率和刺激形态，特别是对于机械性受体如太平洋小体。更多的现代研究侧重于更大、更完整的系统; 通过将动作电位模型与神经系统其他部分的模型(如树突和突触)结合起来，研究人员可以研究神经计算和简单反射，如逃逸反射和其他由中枢模式发生器控制的反射。进入，PA 进入 See also Anode break excitation Bioelectricity Biological neuron model Bursting Central pattern generator Chronaxie Frog battery Neural accommodation Single-unit recording Soliton model in neuroscience Anode break excitation Bioelectricity Biological neuron model Bursting Central pattern generator Chronaxie Frog battery Neural accommodation Single-unit recording Soliton model in neuroscience 阳极破坏兴奋生物电生物神经元模型爆裂中央模式发生器慢性抑制青蛙电池神经调节金钱本色孤子模型神经科学 Notes References Footnotes Journal articles Books Books Web pages Further reading = 进一步阅读 = External links Ionic flow in action potentials at Blackwell Publishing Action potential propagation in myelinated and unmyelinated axons at Blackwell Publishing Generation of AP in cardiac cells and generation of AP in neuron cells Resting membrane potential from Life: The Science of Biology, by WK Purves, D Sadava, GH Orians, and HC Heller, 8th edition, New York: WH Freeman, . Ionic motion and the Goldman voltage for arbitrary ionic concentrations at The University of Arizona A cartoon illustrating the action potential Action potential propagation Production of the action potential: voltage and current clamping simulationshttps://en.wikipedia.org/wiki/Defekte_Weblinks?dwl={{{url}}} Seite nicht mehr abrufbar], Suche in Webarchiven: Kategorie:Wikipedia:Weblink offline (andere Namensräume)[http://timetravel.mementoweb.org/list/2010/Kategorie:Wikipedia:Vorlagenfehler/Vorlage:Toter Link/URL_fehlt Open-source software to simulate neuronal and cardiac action potentials at SourceForge.net Introduction to the Action Potential, Neuroscience Online (electronic neuroscience textbook by UT Houston Medical School) Khan Academy: Electrotonic and action potential Ionic flow in action potentials at Blackwell Publishing Action potential propagation in myelinated and unmyelinated axons at Blackwell Publishing Generation of AP in cardiac cells and generation of AP in neuron cells Resting membrane potential from Life: The Science of Biology, by WK Purves, D Sadava, GH Orians, and HC Heller, 8th edition, New York: WH Freeman, . Ionic motion and the Goldman voltage for arbitrary ionic concentrations at The University of Arizona A cartoon illustrating the action potential Action potential propagation Production of the action potential: voltage and current clamping simulations Open-source software to simulate neuronal and cardiac action potentials at SourceForge.net Introduction to the Action Potential, Neuroscience Online (electronic neuroscience textbook by UT Houston Medical School) Khan Academy: Electrotonic and action potential 布莱克威尔出版社动作电位中的离子流 布莱克威尔出版社有髓和无髓鞘轴突中的动作电位传播 心肌细胞中 AP 的生成和神经细胞中 AP 的生成 生命的膜电位: 生物学，作者: WK Purves，d Sadava，GH，and HC，第8版，纽约: WH Freeman，。动作电位的产生: 电压和电流箝位模拟开源软件模拟神经元和心脏动作电位 Category:Capacitors Category:Neural coding Category:Electrophysiology Category:Electrochemistry Category:Computational neuroscience Category:Cellular neuroscience Category:Cellular processes Category:Membrane biology Category:Plant cognition Category:Action potentials 类别: 电容器类别: 神经编码类别: 电生理学类别: 电化学类别: 计算神经科学类别: 细胞神经科学类别: 细胞过程类别: 膜生物学类别: 植物认知类别: 动作电位 This page was moved from wikipedia:en:Action potential. Its edit history can be viewed at 动作电位/edithistory