动作电位

此词条由神经系统中的动力学模型读书会词条梳理志愿者 okxy 翻译审校，未经专家审核，带来阅读不便，请见谅。

当动作电位（神经冲动）沿着轴突传导时，轴突的跨膜的极性发生变化。响应来自其他神经元的信号，Na⁺ 和 K⁺ 门控的离子通道随着膜电位达到其阈值电位而打开和关闭。动作电位开始时 Na⁺ 通道打开，Na⁺ 进入轴突，导致去极化。当 K⁺ 通道打开而 K⁺ 移出轴突时，就会发生复极化，从而在细胞的外部和内部之间产生极性变化。神经脉冲仅在一个方向上沿着轴突行进，到达轴突末端，在那里它向其他神经元发出信号。

生理学上，动作电位（action potential, AP）就是特定细胞位置的膜电位迅速上升又迅速下降的过程 ：这种去极化会导致相邻位置同样地去极化。动作电位可在神经元、肌肉细胞、内分泌细胞等类型的称为可兴奋细胞（excitable cells）的动物细胞以及某些植物细胞中发生。

在神经元中，动作电位在细胞与细胞之间的通讯中起着中心作用，它可以以跳跃式传导（saltatory conduction ）方式，协助神经信号沿着轴突向位于轴突末端的突触结传播； 然后信号通过突触传递到其他神经元、运动细胞或腺体。在其他类型的细胞中，它们的主要功能是激活细胞内的反应过程。例如，在肌肉细胞中，动作电位是引起肌肉收缩的一系列事件的第一步。在胰腺的 β 细胞中，它们会刺激胰岛素的释放。神经元的动作电位也被称为“神经冲动（neural impulse）”或“脉冲（spike）”，神经元产生的动作电位的时间序列被称为“动作电位序列（spike train）”。神经元发出动作电位或神经冲动，也常说神经在“发放（fire）”。

动作电位是由细胞质膜内嵌的特殊类型的电压门控离子通道（voltage-gated ion channel）产生的。这些通道在膜电位处于细胞的静息电位（一个负数数值）附近时关闭，而在膜电位增加到精确定义的阈电位（threshold voltage）时迅速打开，从而使膜电位去极化。开放状态的通道让钠离子内流，改变电化学梯度，进而使膜电位趋升于零。这便导致更多的通道打开，产生更大的跨膜电流……这个过程爆发性地发生，直到所有可用的离子通道都打开，从而导致膜电位的大幅上升。钠离子的快速内流导致细胞质膜极性反转，随后离子通道迅速失活。随着钠离子通道的关闭，钠离子不再能进入神经元，然后以主动运输的方式被转运到质膜外。随后，钾离子通道被激活，产生一个外向的钾离子电流，使电化学梯度回到静息状态。动作电位发生后，会有短暂的负移，称为后超极化（afterhyperpolarization）。

动物细胞中存在两种基本类型的动作电位。一种是电压门控钠通道产生的，另一种是电压门控钙通道产生的。钠脉冲通常持续不到一毫秒，而钙脉冲可持续 100 毫秒甚至更长时间。在某些类型的神经元，持续稍久的钙脉冲为钠脉冲的长时间迸发提供驱动力。另一方面，在心肌细胞，初始的快速钠脉冲像“点火器”一样，迅速引发钙脉冲，从而产生肌肉收缩。

概述

典型的动作电位波形。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。

动物、植物和真菌的细胞膜几乎都在细胞外部和内部维持一个电压差，称为膜电位（membrane potential）。动物细胞的跨膜电压一般是 -70 mV。这意味着细胞内部相对于外部存在一个负电压。在大多数类型的细胞中，膜电位通常相当稳定。而某些类型的细胞具有电活性，即它们的电压随着时间而波动。在某些类型的有电活性的细胞，包括神经元和肌肉细胞中，电压波动的通常形式为迅速上升而后迅速下降。这些升降的循环即为动作电位。在某些类型的神经元中，整个升降循环在千分之几秒内发生。在肌肉细胞中，典型的动作电位持续时间约为五分之一秒。在其他类型的细胞和植物中，动作电位可能持续三秒或更长时间。

细胞的电特性是由细胞周围的质膜的结构决定的。细胞膜由内嵌更大的蛋白质分子的脂双分子层组成。这种脂双分子层对带电离子的运动产生很强的阻力，因此产生绝缘作用。而质膜内嵌的大蛋白质可作离子的跨膜通道。驱动动作电位的通道蛋白随细胞内外电压差的变化，而在闭合和开放状态的构象之间转换。这些电压敏感蛋白被称为电压门控离子通道。

典型的神经元过程

典型动作电位的近似图显示了动作电位经过细胞膜上一点时的各个阶段。膜电位开始时（时间零点）约为−70 mV。在时间 = 1 ms 时施加刺激，这会将膜电位提高到 −55 mV（阈值电位）以上。施加刺激后，膜电位在时间= 2 ms 时迅速上升到 +40 mV 的峰值电位。在时间 = 3 ms 时膜电位又快速下降并过冲至 −90 mV，最后在时间 = 5 ms 时重新建立 −70 mV 的静息电位。

动物身体组织中的细胞都是电极化的——换句话说，它们维持一个跨细胞质膜的电压差，即所谓的膜电位。这种电极化是嵌入在质膜的蛋白质结构（称为离子泵和离子通道）之间复杂的相互作用中产生的。神经元细胞膜上的离子通道在不同的细胞部位而类型不同，因而树突、轴突和胞体具有不同的电特性。因此，神经元质膜仅在某些部位是可兴奋的（能够产生动作电位）。近年的研究表明，神经元最易兴奋的部位是轴丘（轴突出离胞体的部位）后的部位，称为轴突始段（axonal initial segment），但在大多数情况下轴突和胞体也是可兴奋的。

可兴奋的细胞膜片都有两个重要的膜电位：未受干扰时细胞维持的静息电位（resting potential），和更高值的阈电位。典型神经元的轴丘的静息电位约为 -70 mV，阈值电位约为 -55 mV。神经元的突触输入导致膜去极化或超极化，即它们使膜电位升高或降低。当去极化累积到足以使膜电位达到阈电位时，就会触发动作电位。动作电位被触发时，膜电位猝然上升，随后同样猝然下降，且常降到静息电位以下一段时间。动作电位的波形是固定不变的，这意味着在给定的细胞中，所有动作电位的升降幅度和时间过程大致相同（本文后面将讨论例外情况）。在大多数神经元中，整个过程发生在千分之一秒左右。很多类型的神经元不断地以每秒 10-100 次的速度发放动作电位。而有些类型更安静的细胞，可能持续几分钟或更长时间而不发生任何动作电位。

生物物理基础

动作电位因细胞膜上特殊类型的电压门控离子通道产生 。电压门控离子通道是一种跨膜蛋白，有三关键性质：

1. 它能够呈现多种构象。
2. 至少一种构象能在膜上形成通道，以渗透特定种类的离子。
3. 构象之间的转换受到膜电位的影响。

因此，电压门控离子通道在膜电位处于某些水平时倾向于打开，在其他水平时倾向于关闭。然而，膜电位和离子通道的状态之间在大多数情况下是一种概率关系，并且存在时间延迟。离子通道在不可预测的时间在不同构象之间切换：膜电位决定状态切换速率和单位时间每种切换类型的概率。

Action potential propagation along an axon沿着轴突的动作电位传导

电压门控离子通道能够产生动作电位，是因为它们能够产生正反馈回路：膜电位控制离子通道的状态，而离子通道的状态控制膜电位。因此，在某些情况下，膜电位的上升会导致离子通道打开，又导致膜电位的进一步上升。当这种正反馈循环（Hodgkin 循环）爆发性地进行时，就会产生动作电位。电压门控离子通道的生物物理特性决定了动作电位的时间和幅度轨迹。存在几种能产生动作电位所必需的正反馈回路的离子通道。电压门控性钠通道负责神经传导的快速动作电位。肌细胞和某些类型的神经元的稍慢的动作电位是由电压门控钙通道产生的。每种类型都有多种变体，具有不同的电压灵敏度和不同的时间动力学。

研究最多的电压依赖型离子通道是快速神经传导中的钠通道。这些钠离子通道有时被称为 Hodgkin-Huxley 钠离子通道，因为它们是 Alan Hodgkin 和 Andrew Huxley 在他们获得诺贝尔奖的关于动作电位的生物物理研究中首先描述的，但更方便地被称为 Na_V 通道（“ v”代表“电压”）。Na_V 通道有三种可能的状态，即失活（deactivated）、激活（activated）和灭活（inactivated）。这些通道处于激活状态时，允许钠离子通过。当膜电位低时，通道大部分时间处于失活（关闭）状态。如果膜电位升高到某一水平以上，通道转换到激活（开放）状态的概率增加。膜电位越高，激活的可能性就越大。通道一旦被激活，最终会转换到灭火（关闭）状态，并倾向在一段时间内保持灭活状态；如果膜电位再次变低，通道最终会转换到失活状态。在动作电位发生过程中，大多数这种类型的通道经历失活→激活→灭活→失活的循环过程。然而这只是群体平均行为——理论上单个通道可在任何时刻发生任何转换。然而，通道从灭活状态直接转换到激活状态的概率极低：处于灭活状态的通道是不应的，直到它回到灭活状态。

这些的结果是，Na_V 通道的动力学决定于状态转换矩阵，其中转换速率以一种复杂的方式依赖于电压。由于这些通道本身在决定电位中起着重要作用，系统的全局动力学可能很难计算出来。为了解决这个问题，Hodgkin 和 Huxley 为决定离子通道状态的参数建立了一组微分方程，称为 Hodgkin-Huxley 方程（Hodgkin-Huxley equations）。这些方程在后续的研究被修正了很多，但构成很多动作电位生物物理学的理论研究的起点。

动作电位过程中的离子移动。图注：a）钠离子（Na⁺）、b）钾离子（K⁺）、c） 钠通道、d）钾通道、e）钠钾泵。 在动作电位发生的过程中，神经元质膜的通透性发生变化。在静息状态（1），钠离子和钾离子能有限地跨膜通过，神经元内部具有净负电荷。一旦触发动作电位，神经元去极化（2）激活钠通道，允许钠离子通过细胞膜进入细胞，导致神经元相对于细胞外液的净正电荷。达到动作电位峰值后，神经元开始复极化（3），其中钠通道关闭，钾通道打开，允许钾离子穿过膜进入细胞外液，使膜电位恢复为负值。最后，有一个不应期（4），在此期间，电压依赖的离子通道失活，而 Na⁺ 和 K⁺ 离子返回到其在膜上的静息状态分布（1），并且神经元准备重复该过程产生下一个动作电位。

随着膜电位的增加，钠离子通道打开，允许钠离子进入细胞。随后钾离子通道打开，允许钾离子流出细胞。钠离子内流增加了细胞中带正电荷的阳离子的浓度，导致去极化，这时细胞的电位高于细胞的静息电位。钠离子通道在动作电位峰值处关闭，而钾离子继续流出细胞。钾离子外流会降低细胞的膜电位或使细胞超极化。膜电位比静息电位高一点时，钾电流超过钠电流，而恢复到正常的静息值，通常为 -70 mV。然而，如果电位增加超过一个关键阈值，通常高于静息值 15 mV，钠电流将占主导地位。这就导致了一种失控的情况，即钠电流的正反馈激活了更多的钠通道。因此，细胞发放，产生动作电位。神经元诱发动作电位的频率通常被称为发放频率或神经放电频率。

在动作电位过程中，电压门控通道的开放所产生的电流通常明显大于起初的刺激电流。因此，动作电位的幅度、持续时间和波形在很大程度上取决于可兴奋膜的性质，而不是刺激的幅度或持续时间。动作电位的这种全或无的特性使它有别于受体电位（receptor potentials）、电紧张电位（electrotonic potentials）、阈下膜电位振荡（subthreshold membrane potential oscillations）和突触电位（synaptic potentials）等随刺激强度变化的级量电位。取决于电压门控通道的类型、漏电通道、通道分布、离子浓度、膜电容、温度等因素，许多细胞类型和细胞分区中存在多种动作电位类型。

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

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

在 Hodgkin-Huxley 膜电容模型中，动作电位的传输速度没有定义，而是假设附近区域受邻近通道释放的离子干扰而去极化。离子扩散和半径的测量表明这是不可能的。此外，对熵变和时序的测量中的矛盾，对电容模型是独立工作的产生质疑。另外，Gilbert Ling 的吸附假说认为活细胞的膜电位和动作电位是由于活动离子吸附在细胞的吸附位点上.。

动作电位的电性质的成熟

神经元产生和传播动作电位的能力在发育过程中发生变化。神经元在电流脉冲作用下的膜电位变化量是膜输入电阻的函数。随着细胞的生长，膜上添加了更多的通道，导致输入电阻减小。一个成熟的神经元在突触电流的作用下，膜电位也会发生更短时间的变化。雪貂外侧膝状核的神经元在 P0 时比在 P30 时有更长的时间常数和更大的电压偏转 。动作电位持续时间减少的一个后果是，可以保持高频刺激的反应信号的保真度。高频刺激后，未成熟神经元更容易发生突触抑制而非增强 。

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（Xenopus）神经元最初的动作电位需要 60-90 毫秒。在发育过程中，这个时间减少到 1 毫秒。这种急剧下降有两个原因。首先，向内的电流主要由钠离子通道输送 。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 。

为了使钙离子依赖的动作电位转变为钠离子依赖的动作电位，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的表达中发挥作用。如果阻断非洲爪蟾心肌细胞的动作电位，通常发生的钠和钾电流密度增加就会被阻止或延迟 。

在不同物种中都可观察到这种电特性的成熟过程。非洲爪蟾的钠和钾电流在神经元进入有丝分裂的最后时相后急剧增加。大鼠大脑皮层神经元的钠电流密度在刚出生的 2 周内增加 600% 。

神经传递

神经元的解剖学

有几类细胞可以产生动作电位，比如植物细胞、肌肉细胞和心脏中的特化细胞（在这些细胞中发生心脏动作电位）。然而，最主要的兴奋性细胞是神经元，其亦具有最简单的动作电位机制。

神经元是电兴奋型细胞，一般包含一个或多个树突、一个胞体、一个轴突以及一个或多个轴突末梢。树突是细胞的突起，其主要功能是接收突触信号。突触上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。其上分布有高密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。这确保树突棘内部发生的变化不太可能影响邻近的树突棘。树突棘除了极少数例外情况（见 LTP），可以作为一个独立的单位工作。树突从胞体延伸出来，胞体是细胞核和许多“正常”的真核细胞器的所在。与树突棘不同，胞体的表面布满了电压可激活的离子通道。这些通道帮助传输由树突产生的信号。从胞体延伸出来的是轴丘。这个区域的特征是有非常高浓度的电压激活钠离子通道。一般认为它是动作电位的起始区，或触发区。在树突棘处产生的多个信号，经胞体传输而汇聚于此。轴丘之后便是轴突。这是一个从胞体中延伸出来的细管状突起。轴突被髓鞘（myelin）绝缘。髓鞘由神经胶质细胞组成，在外周神经系统是施万细胞，在中央神经系统为少突胶质细胞。虽然神经胶质细胞不参与电信号的传递，但可以与神经元通讯和提供重要的生化支持。具体来说，髓鞘绕着轴突多重包裹，形成一层厚厚的脂肪层，阻止离子进入或逃离轴突。这种绝缘可以避免信号发生剧烈的衰减，并确保信号更快速地传播；但同时会限制轴突表面，使其没有离子通道。因此，在轴突上每隔一段就会有块不带绝缘层的膜片。这些郎飞结（nodes of Ranvier）可以被认为是“迷你轴丘”，因为其目的是增强信号，以避免明显的信号衰减。在最远端，轴突失去绝缘的髓鞘，并开始分支成几个轴突末梢。这些突触前末梢，或称突触结（synaptic bouton），是突触前细胞轴突内的一个特殊区域，其中包含神经递质，这些神经递质被包装在称为突触小泡的膜包裹的小球内。

发生

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.

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. 当动作电位传至突触前轴突末端（上部）时，它会导致神经递质分子的释放，这些分子打开突触后神经元中的离子通道（底部）。这些输入引起的兴奋性和抑制性突触后电位，在突触后神经元中整合引起新的动作电位。

在认识动作电位沿轴突的传播并止于突触结之前，可以了解一下动作电位是如何轴丘处引发的。基本的要求就是把轴丘的膜电位抬高到动作电位发放的域值之上。存在几种去极化的方式。

动力学

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.

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

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“全或无”原理

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.

动作电位的幅度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。 这与受体电位不同，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 感觉神经元

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.

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，或者转换成连续级量的电位，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的细胞（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的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 起搏电位

In pacemaker potentials, the cell spontaneously depolarizes （straight line with upward slope） until it fires an action potential. 在起搏电位中，细胞自发地去极化（具有向上斜率的直线），直到它发放动作电位。

In sensory neurons, action potentials result from an external stimulus. However, some excitable cells require no such stimulus to fire: They spontaneously depolarize their axon hillock and fire action potentials at a regular rate, like an internal clock. The voltage traces of such cells are known as pacemaker 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，一些兴奋型细胞不需要这样的刺激就可以发放动作电位：它们自发地使轴丘去极化，并以一个规律的速率发放动作电位，就像一个内部时钟。这种细胞的电压描记称为起搏电位。心脏窦房结的心律起搏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频率。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

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.

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. T。因此，膜电位影响渗透性，进而进一步影响膜电位。这就为正反馈提供了可能性，而正反馈是动作电位上升阶段的关键部分。一个复杂的因素是，单个离子通道可能有多个内部“门”，以相反的方式或不同的速率响应 Vm 中的变化.模板:Sfnm F。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.

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, f。，并因此在1963年获得了诺贝尔生理学或医学奖动作电位奖523. 然而，他们的模型只考虑了两种类型的电压敏感离子通道，并对它们做出了几个假设，例如，它们的内部门的开启和关闭是相互独立的。实际上，离子通道有很多种类型，戈尔丁通道和铝通道s, a，它们并不总是独立开启和关闭的y.。

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.

= = = 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

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

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

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

= = = = 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.

= = = 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.

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.

*

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

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 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e. 。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.

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.

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, t，但是参见第一个关于跳跃式传导的实验证据来自 Ichiji Tasaki 和 Taiji Takeuchi < br/> Tasaki，i ani in 和来自 Andrew Huxley 和 Robert Stämpflii. B。相比之下，在无髓鞘的轴突中，动作电位在紧邻的膜上激发了另一个动作电位，并像波一样不断地沿着轴突移动。

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. 比较猫中髓鞘和无髓鞘轴突s的传导速度。模板：Sfn 髓鞘神经元的传导速度 v 与轴突直径 d（即 v ∝ d）大致呈线性变化，[lower-alpha 1] 而无髓鞘神经元的速度大致与平方根 （v ∝模板：Radic） 一样变化。[下阿尔法2]红色和蓝色曲线是实验数据的拟合，而虚线是它们的理论推断。

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. Co。相反，对于一定的传导速度，有髓纤维比无髓纤维小。例如，在有髓青蛙轴突和无髓青蛙轴突中，动作电位的移动速度大致相同（25米/秒），但是青蛙轴突的直径要小30倍，横截面积要小1000倍。此外，由于离子电流仅限于郎飞结，跨膜“泄漏”的离子要少得多，从而节省了新陈代谢能量。这种节省是一个重大的选择优势，因为人类神经系统消耗大约20% 的身体代谢能量.。

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

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.

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t.

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

= = = = 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ble a，并在1946年被 Hodgkin 和 Rushton 证明与神经元有关6. 。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

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

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 \,

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

\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.

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

Termination 终止

Chemical synapses化学突触

In general, action potentials that reach the synaptic knobs cause a neurotransmitter to be released into the synaptic cleft. 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

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

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.。

Other cell types 其他细胞类型

Cardiac action potentials 心肌动作电位

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. 心脏动作电位的阶段。电压的急剧上升（“0”）对应于钠离子的流入，而两个衰变（分别为“1”和“3”）对应于钠通道失活和钾离子的再极化流。特征性平台（“2”）是由电压敏感钙通道的打开引起的。

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.

心脏动作电位在协调心脏收缩中起着重要作用。窦房结的心脏细胞提供了同步心脏的起搏器电位t.。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

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.

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

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.

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.

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.

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）.。神经细胞膜上的电位。的静息电位可以更容易地激活动作电位。因此，当一只昆虫落在植物的陷阱上时，它就会触发一个毛发样的机械感受器。. 低这个受体激活一个持续约1.5毫秒的动作电位. 。最终，这会导致钙离子进入细胞，使细胞稍微去极化。 https://www.ncbi.nlm.nih.gov/books/nbk11069/

However, the flytrap doesn't close after one trigger. Instead, it requires the activation of 2 or more hairs. 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.

随着随后释放的阳性钾离子，动作电位在植物中涉及盐（KCl）渗透损失。然而，动物的动作电位是渗透中性的，因为等量的钠进入和钾离开相互抵消渗透。植物细胞s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.

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

不同于上升

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

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动物的代表性横切的动作电位的比较

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

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.

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

Giant axons of the longfin inshore squid （Doryteuthis pealeii） were crucial for scientists to understand the action potential.长鳍近海鱿鱼（Doryteuthis pealeii）的巨型轴突对于科学家了解动作潜力至关重要。[注1]

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.

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e. 。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 I_C 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 V_m, the solution was to design a circuit that kept V_m fixed （zero rate of change） regardless of the currents flowing across the membrane. Thus, the current required to keep V_m at a fixed value is a direct reflection of the current flowing through the membrane. Other electronic advances included the use of Faraday cages and electronics with high input impedance, so that the measurement itself did not affect the voltage being measured.模板:Sfn

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.

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.

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.

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.

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历史

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. 两个浦肯野细胞的图像（标记为A），由圣地亚哥·拉蒙·卡哈尔于1899年绘制。大树状树状的树状物进入索玛，从中出现单个轴突，并通常向下移动，并带有几个分支点。标记B的较小细胞  是颗粒细胞s。

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

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.

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. T。凯瑟琳 · m · 奥列斯科和弗雷德里克 · l · 福尔摩斯。“实验、量化与发现: 亥姆霍兹早期生理学研究，1843-50”。在《赫尔曼·冯·亥姆霍兹和19世纪科学的基础》，ed。大卫 · 卡汉，50-108。伯克利; 洛杉矶; 伦敦: 加州大学，1994年。为了证明神经组织是由离散的细胞组成的，西班牙物理学家圣地亚哥·拉蒙-卡哈尔和他的学生们使用了 Camillo Golgi 开发的染色剂来显示神经元的无数形状，他们煞费苦心地进行了渲染。由于他们的发现，高尔基和拉蒙 · 卡哈尔获得了1906年的诺贝尔生理学奖. 。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. 钠钾泵在其E2-Pi状态下的带状图。脂质双层的估计边界显示为蓝色（细胞内）和红色（细胞外）平面。

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.

20世纪是电生理的重要时期。1902年和1912年，Julius Bernstein 提出了动作电位是由轴突膜对离子的渗透性改变引起的假说.。Ken Cole 和 Howard Curtis 证实了 Bernstein 的假说，他们发现在动作电位期间膜电导增加. 。1907年，Louis Lapicque 提出，动作电位产生的阈值被跨越, w，后来被证明为离子电导动力学系统的乘积。1949年，Alan Hodgkin 和 Bernard Katz 完善了 Bernstein 的假说，他们认为轴突膜对不同的离子可能有不同的通透性; 特别是，他们证明了钠通透性对动作电位的关键作用. 。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. 。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s 和冷冻电子显微研究s.。

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 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7，它的性质逐渐被阐明, culm，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

Equivalent electrical circuit for the Hodgkin–Huxley model of the action potential. I_m and V_m represent the current through, and the voltage across, a small patch of membrane, respectively. The C_m represents the capacitance of the membrane patch, whereas the four g's represent the 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. 作用电位的霍奇金-赫胥黎模型的等效电路。I_m 和 V_m 分别表示通过一小块膜的电流和两端的电压。C_m代表膜贴片的电容，而四g代表四种离子的电导率。左边的两个电导，钾（K）和钠（Na），用箭头显示，表明它们可以随着施加的电压而变化，对应于电压敏感的离子通道。右侧的两个电导有助于确定静息膜电位。

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.

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,模板:Sfn s，但与实际存在的神经膜相比，它的局限性很小s，其复杂性激发了几个更简化的模型，例如 Morris-Lecar 模型l a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l,， 已经在数学中得到了很好的研究, c，computationn Nelson，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.。

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

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

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