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[[File:Action Potential.gif|thumb|upright=1.5|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。|链接=Special:FilePath/Action_Potential.gif]]

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生理学上，动作电位（action potential, AP）就是特定细胞位置的膜电位迅速上升又迅速下降的过程<ref name=":3">{{cite journal | vauthors = Hodgkin AL, Huxley AF | title = A quantitative description of membrane current and its application to conduction and excitation in nerve | journal = The Journal of Physiology | volume = 117 | issue = 4 | pages = 500–44 | date = August 1952 | pmid = 12991237 | pmc = 1392413 | doi = 10.1113/jphysiol.1952.sp004764 }}</ref> ~~：这种去极化会导致相邻位置同样地去极化。动作电位可在神经元、肌肉细胞、内分泌细胞等类型的称为可兴奋细胞（excitable~~ cells）的动物细胞以及某些植物细胞中发生。

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生理学上，动作电位（action potential, AP）就是特定细胞位置的膜电位迅速上升又迅速下降的过程<ref name=":3">{{cite journal | vauthors = Hodgkin AL, Huxley AF | title = A quantitative description of membrane current and its application to conduction and excitation in nerve | journal = The Journal of Physiology | volume = 117 | issue = 4 | pages = 500–44 | date = August 1952 | pmid = 12991237 | pmc = 1392413 | doi = 10.1113/jphysiol.1952.sp004764 }}</ref> ：这种去极化（depolarization）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兴奋性细胞（excitable cells）的动物细胞以及某些植物细胞中发生。

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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扣结（synaptic bouton 或 synaptic knob）传播；然后信号通过突触传递到其他神经元、运动细胞或腺体。在其他类型的细胞中，它们的主要功能是激活细胞内的反应过程。例如，在肌肉细胞中，动作电位是引起肌肉收缩的一系列事件的第一步。在胰腺的 β 细胞中，它们会刺激胰岛素的释放<ref name="pmid16464129" group="lower-alpha">{{cite journal | vauthors = MacDonald PE, Rorsman P | title = Oscillations, intercellular coupling, and insulin secretion in pancreatic beta cells | journal = PLOS Biology | volume = 4 | issue = 2 | pages = e49 | date = February 2006 | pmid = 16464129 | pmc = 1363709 | doi = 10.1371/journal.pbio.0040049 }} {{open access}}</ref>。神经元的动作电位也被称为“神经冲动（neural impulse）”或“脉冲（spike）”，神经元产生的动作电位的时间序列被称为“动作电位序列（spike train）”。神经元发出动作电位或神经冲动，也常说神经在“发放（fire）”。

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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扣结（synaptic bouton 或 synaptic knob）传播（propagation）；然后信号通过突触传递到其他神经元、运动细胞或腺体。在其他类型的细胞中，它们的主要功能是激活细胞内的反应过程。例如，在肌肉细胞中，动作电位是引起肌肉收缩的一系列事件的第一步。在胰腺的 β 细胞中，它们会刺激胰岛素的释放<ref name="pmid16464129" group="lower-alpha">{{cite journal | vauthors = MacDonald PE, Rorsman P | title = Oscillations, intercellular coupling, and insulin secretion in pancreatic beta cells | journal = PLOS Biology | volume = 4 | issue = 2 | pages = e49 | date = February 2006 | pmid = 16464129 | pmc = 1363709 | doi = 10.1371/journal.pbio.0040049 }} {{open access}}</ref>。神经元的动作电位也被称为“神经冲动（neural impulse）”或“脉冲（spike）”，神经元产生的动作电位的时间序列被称为“动作电位序列（spike train）”。神经元发出动作电位或神经冲动，也常说神经在“发放（fire）”。

动作电位是由细胞质膜内嵌的特殊类型的电压门控离子通道（voltage-gated ion channel）产生的<ref name="pmid17515599" group="lower-alpha">{{cite journal | vauthors = Barnett MW, Larkman PM | title = The action potential | journal = Practical Neurology | volume = 7 | issue = 3 | pages = 192–7 | date = June 2007 | pmid = 17515599 | url = http://pn.bmj.com/content/7/3/192.short | url-status = live | archive-url = https://web.archive.org/web/20110708074452/http://pn.bmj.com/content/7/3/192.short | df = dmy-all | archive-date = 8 July 2011 }}</ref>。这些通道在膜电位处于细胞的静息电位（一个负数数值）附近时关闭，而在膜电位增加到精确定义的阈电位（threshold voltage）时迅速打开，从而使膜电位去极化<ref name="pmid17515599" group="lower-alpha" />。开放状态的通道让钠离子内流，改变电化学梯度，进而使膜电位趋升于零。这便导致更多的通道打开，产生更大的跨膜电流……这个过程爆发性地发生，直到所有可用的离子通道都打开，从而导致膜电位的大幅上升。钠离子的快速内流导致细胞质膜极性反转，随后离子通道迅速失活。随着钠离子通道的关闭，钠离子不再能进入神经元，然后以主动运输的方式被转运到质膜外。随后，钾离子通道被激活，产生一个外向的钾离子电流，使电化学梯度回到静息状态。动作电位发生后，会有短暂的负移，称为后超极化（afterhyperpolarization）。

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===典型的神经元过程===

[[File:Action potential.svg|thumb|300px|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。|链接=Special:FilePath/Action_potential.svg]]

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动物身体组织中的细胞都是电极化的——换句话说，它们维持一个跨细胞质膜的电压差，即所谓的膜电位。这种电极化是嵌入在质膜的蛋白质结构（称为离子泵和离子通道）之间复杂的相互作用中产生的。神经元细胞膜上的离子通道在不同的细胞部位而类型不同，因而树突、轴突和胞体具有不同的电特性。因此，神经元质膜仅在某些部位是可兴奋的（能够产生动作电位）。近年的研究表明，神经元最易兴奋的部位是轴丘（轴突出离胞体的部位）后的部位，称为轴突始段（axonal initial segment），但在大多数情况下轴突和胞体也是可兴奋的<ref name=":6">{{cite journal | vauthors = Leterrier C | title = The Axon Initial Segment: An Updated Viewpoint | journal = The Journal of Neuroscience | volume = 38 | issue = 9 | pages = 2135–2145 | date = February 2018 | pmid = 29378864 | pmc = 6596274 | doi = 10.1523/JNEUROSCI.1922-17.2018 }}</ref>。

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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（axon hillock，轴突出离胞体的部位）后的部位，称为轴突始段（axonal initial segment），但在大多数情况下轴突和胞体也是可兴奋的<ref name=":6">{{cite journal | vauthors = Leterrier C | title = The Axon Initial Segment: An Updated Viewpoint | journal = The Journal of Neuroscience | volume = 38 | issue = 9 | pages = 2135–2145 | date = February 2018 | pmid = 29378864 | pmc = 6596274 | doi = 10.1523/JNEUROSCI.1922-17.2018 }}</ref>。

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

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动作电位沿轴突传播并终于突触扣结之前，要先在轴丘触发。触发的基本条件就是轴丘的膜电位提高到动作电位发放的域值以上。存在几种去极化的方式。

===动作电位的动力学===

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~~Action potentials are most commonly initiated by [[excitatory~~ postsynaptic potential]]s from a presynaptic neuron.{{sfnm|1a1=Bullock|1a2=Orkand|1a3=Grinnell|1y=1977|1pp=177–240|2a1=Schmidt-Nielsen|2y=1997|2pp=490-499|3a1=Stevens|3y=1966|3p=47–68}} Typically, [[neurotransmitter]] molecules are released by the [[synapse|presynaptic]] [[neuron]]. These neurotransmitters then bind to receptors on the postsynaptic cell. This binding opens various types of [[ion channel]]s. 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 [[spatial summation|work together]] at [[temporal summation|nearly the same time]] to provoke a new action potential. Their joint efforts can be thwarted, however, by the counteracting [[inhibitory postsynaptic potential]]s.

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动作电位多是由突触前神经元引起的兴奋性突触后电位（excitatory postsynaptic potentials）引起的。一般地，神经递质分子由突触前神经元释放后，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，能够改变细胞膜的局部通透性，从而改变膜电位。如果这种结合提高膜电位（去极化），则突触是兴奋性的；而如果这种结合降低膜电位（使细胞膜超极化），它就是抑制性的。无论是升高还是降低，膜电位的变化都会被动传播到邻近区域的膜上（如电缆方程（cable equation ）及其改进所刻画的），并且通常随着与突触的距离以及与神经递质结合后的时间呈现指数衰减。少量兴奋性电位可传至轴丘，并且（在极少情况下）使膜足够去极化以引发新的动作电位。更常见的是，从多个突触传来的兴奋性电位必须几乎同时作用才能引发一个新的动作电位。当然，这种共同作用也可能被反作用的抑制性突触后电位（inhibitory postsynaptic potentials）所阻。

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动作电位经常是突触前神经元引起的的兴奋性突触后电位（excitatory postsynaptic potentials）引起的。通常，神经递质分子由突触前神经元释放后，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，能够改变细胞膜的局部通透性，从而改变膜电位。如果这种结合提高膜电位（去极化），则突触是兴奋性的；而如果这种结合降低膜电位（使细胞膜超极化），它就是抑制性的。无论是升高还是降低，膜电位的变化都会被动地传播到邻近区域的膜上（如电缆方程（[[cable equation]] ）及其改进所描述的），并且通常随着与突触的距离以及与神经递质结合后的时间呈现指数衰减。少量兴奋性电位可能传至轴丘，并且（在极少情况下）使膜足够去极化以引发新的动作电位。更常见的是，从多个突触传来的兴奋性电位必须几乎同时作用才已引发一个新的动作电位。当然，这种共同作用也可能被反作用的抑制性突触后电位（[[inhibitory postsynaptic ~~potential]]s）所阻止。~~

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Neurotransmission can also occur through [[electrical synapse]]s.{{sfnm|1a1=Bullock|1a2=Orkand|1a3=Grinnell|1y=1977|1pp=178–180|2a1=Schmidt-Nielsen|2y=1997|2pp=490-491}} Due to the direct connection between excitable cells in the form of [[gap junction]]s, 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.{{Citation needed|date=May 2011}} Electrical synapses are found in all nervous systems, including the human brain, although they are a distinct minority.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2001}}

神经传导也可通过电突触（electrical synapse）进行。兴奋性细胞之间以缝隙连接（gap junction）的形式直接相连，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单向移动。电突触存在于所有神经系统，包括人脑中，尽管它们只占很少部分。

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动作电位的幅度（amplitude）与引起动作电位的电流的大小无关。换句话说，更大的电流不会产生更大幅度的动作电位。因此，动作电位被称为全或无（all-or-none）信号，因为它们要么完全发生，要么根本不发生。<ref name="Sasaki" group="lower-alpha">Sasaki, T., Matsuki, N., Ikegaya, Y. 2011 Action-potential modulation during axonal conduction Science 331 (6017), pp. 599–601</ref><ref name="Aur" group="lower-alpha">{{cite journal | vauthors = Aur D, Connolly CI, Jog MS | title = Computing spike directivity with tetrodes | journal = Journal of Neuroscience Methods | volume = 149 | issue = 1 | pages = 57–63 | date = November 2005 | pmid = 15978667 | doi = 10.1016/j.jneumeth.2005.05.006 | s2cid = 34131910 }}</ref><ref name="Aur, Jog" group="lower-alpha">Aur D., Jog, MS., 2010 Neuroelectrodynamics: Understanding the brain language, IOS Press, 2010. {{DOI|10.3233/978-1-60750-473-3-i}}</ref> 这与受体电位不同，受体电位的幅度取决于刺激的强度。这两种情况下，动作电位的频率都与刺激的强度相关。

===感觉神经元===

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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.{{sfnm|1a1=Schmidt-Nielsen|1y=1997|1pp=535–580|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2pp=49–56, 76–93, 247–255|3a1=Stevens|3y=1966|3pp=69–79}} 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 [[olfaction|smell]] and [[somatosensory system|touch]], respectively. However, not all sensory neurons convert their external signals into action potentials; some do not even have an axon.{{sfnm|1a1=Bullock|1a2=Orkand|1a3=Grinnell|1y=1977|1pp=53|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2pp=122–124}} Instead, they may convert the signal into the release of a [[neurotransmitter]], or into continuous [[receptor potential|graded potentials]], either of which may stimulate subsequent neuron（s） into firing an action potential. For illustration, in the human [[ear]], [[hair cell]]s convert the incoming sound into the opening and closing of [[stretch-activated ion channel|mechanically gated ion channels]], which may cause [[neurotransmitter]] molecules to be released. In similar manner, in the human [[retina]], the initial [[photoreceptor cell]]s and the next layer of cells （comprising [[bipolar cell]]s and [[horizontal cell]]s） do not produce action potentials; only some [[amacrine cell]]s and the third layer, the [[Retinal ganglion cell|ganglion cell]]s, produce action potentials, which then travel up the [[optic nerve]].

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在感觉神经元（sensory neurons）中，压力、温度、光或声音等外部信号与离子通道的开关相耦联，进而改变细胞膜的离子通透性和电位。这些电位变化可以是兴奋性的（去极化）或抑制性（超极化）的，在某些感觉神经元中，不同突触电位的合力使轴丘足够去极化以引起动作电位。比如分别在人类嗅觉和触觉中至关重要的嗅觉感觉神经元和迈斯纳氏小体（Meissner's corpuscle）。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。而是将信号转换成一种神经递质的释放，或者转换成连续的级量电位，这两种都可以刺激后续的神经元发放动作电位。例如，人耳中的毛细胞将传入的声音转换成机械门控离子通道（mechanically gated ion channels）的开关，这可导致神经递质分子的释放。同样，在人类视网膜中，第一层光敏感的感光细胞以及第二层的双极细胞（bipolar cells）和水平细胞（horizontal cells）不产生动作电位；只有一些无长突细胞（amacrine cell）和第三层的神经节细胞（ganglion cells）产生动作电位，并沿视神经传递。

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在感觉神经元（sensory neurons）中，压力、温度、光或声音等外部信号与离子通道的开关相耦合，进而改变细胞膜的离子通透性及其电位。这些电位变化可以是兴奋性（去极化）或抑制性（超极化）的，在某些感觉神经元中，它们的联合作用可以使轴丘去极化到足够以引起动作电位。人类的一些例子包括嗅觉受器神经元和迈斯纳氏小体（Meissner's corpuscle），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。而是，他们可以将信号转换成一种神经递质的释放，或者转换成连续的级量电位，这两种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（mechanically gated ion channels）的开关，这可以导致神经递质分子的释放。同样，在人类视网膜中，第一层光敏感的感光细胞和第二层的细胞（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（amacrine cell）和第三层的神经节细胞（ganglion cells）产生动作电位，并沿视神经传递。

===起搏电位===

[[文件:Pacemaker potential.svg.png|替代=|缩略图|在起搏电位中，细胞自发地去极化（斜向上的直线），直到它发放动作电位。]]

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

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感觉神经元中，动作电位是由外部刺激引起的。然而，一些兴奋性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，以特定的速率发放动作电位，像内部时钟一样。这种细胞的电位变化称为起搏电位（pacemaker potentials）。心脏窦房结（ sinoatrial node）的心脏起搏细胞（cardiac pacemaker cells）就是一个很好的例子。<ref name="noble_1960" group="lower-alpha">{{cite journal | vauthors = Noble D | title = Cardiac action and pacemaker potentials based on the Hodgkin-Huxley equations | journal = Nature | volume = 188 | issue = 4749 | pages = 495–7 | date = November 1960 | pmid = 13729365 | doi = 10.1038/188495b0 | bibcode = 1960Natur.188..495N | s2cid = 4147174 }}</ref> 虽然这种起搏电位有其自然节奏，但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。外部刺激不是引起细胞动作电位的连续性发放，仅是改变其节奏。某些情况下，存在对发放频率更为复杂的调节，引起特定的动作电位模式，比如爆发（bursting）。

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在感觉神经元中，动作电位是由外部刺激引起的。然而，一些兴奋性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，并像一个内部时钟一样，以特定的速率发放动作电位。这种细胞的电位变化称为起搏电位（pacemaker potentials）。心脏窦房结（ [[sinoatrial node]]）的心脏起搏细胞（cardiac pacemaker cells）就是一个很好的例子。<ref name="noble_1960" group="lower-alpha" /> 虽然这种起搏电位有其自然节奏，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连续性动作电位，只是改变其发放频率。对发放频率的调节，在某些情况中可能更复杂，引起特定发放模式，如爆发（bursting）。

==动作电位的相位==

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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 (physiology)|refractory period]], which may overlap with the other phases.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|p=38}}

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动作电位可分为五个阶段：上升相（the rising phase）、峰值相（the peak phase）、下降相（the falling phase）、下冲相（the undershoot phase）和不应期（the refractory period）。在上升相，膜电位去极化（正向变化）。去极化停止的点称为峰值相。在这个阶段，膜电位达到了最大值。在这之后就是下降相，膜电位负向变化，下降趋于静息电位。下冲（undershoot）或后超极化（afterhyperpolarization）相是膜电位短暂变得比静息时还负（超极化）的时期。最后，不能或很难继续发放动作电位的时期被称为不应期，可与其他阶段存在重叠。

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动作电位可分为五个阶段：上升相（the rising phase）、峰值相（the peak phase）、下降相（the falling phase）、下冲相（the undershoot phase）和不应期（the refractory period）。在上升相，膜电位去极化（正向变化）。去极化停止的点称为峰值相。在这个阶段，膜电位达到了最大值。在这之后就是下降相，膜电位变得更负，降向静息电位。下冲（undershoot）或后超极化（[[afterhyperpolarization]]）相是膜电位暂时变得比静息时还负的时期（超极化）。最后，不能或很难继续发放动作电位的时间被称为不应期，可能与其他阶段有重叠。

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

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动作电位的过程是由两个耦合的效应决定的。首先，膜电位的变化引起电压敏感离子通道的开关，进而改变了膜对这些离子的渗透性。其次，根据戈德曼方程（[[Goldman equation]]），这种渗透率的变化改变了平衡电位 ''Em''，从而改变了膜电位。<ref name="goldman_1943" group="lower-alpha" /> 因此，膜电位影响渗透性，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相的关键。令事情更复杂的是，一个离子通道内可能有多个“门”，对 ''Vm'' 以相反的方式或不同速率做出反应。<ref name="hodgkin_1952" group="lower-alpha" /> 例如，尽管提高 ''Vm'' 能打开电压敏感钠通道中的大多数门，但它也缓慢地关闭通道的“失活门”。因此，当 ''Vm'' 突然升高时，钠离子通道开始打开，但随后随着较慢的失活而关闭。

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~~The voltages and currents of the action potential in all of its phases were modeled accurately by~~ [[~~Alan Lloyd Hodgkin~~]] ~~and [[Andrew Huxley]] in 1952,~~<ref name="~~hodgkin_1952~~" group=lower-alpha /> ~~for which they were awarded the [[Nobel Prize~~ in Physiology ~~or Medicine]] in 1963~~.<ref name="~~Nobel_1963~~" group=lower-~~Greek~~>{{cite ~~press release~~ | ~~url~~ = ~~http://nobelprize.org/nobel_prizes/medicine/laureates/1963/index.html~~ | title = ~~The Nobel Prize~~ in ~~Physiology or Medicine 1963~~ | ~~publisher~~ = The ~~Royal Swedish Academy~~ of ~~Science~~ | ~~year~~ = ~~1963~~ | ~~access-~~date = ~~2010-02-21~~ | ~~url-status~~ = ~~live~~ | ~~archive-url~~ = ~~https://web~~.~~archive.org~~/~~web/20070716195411/http://nobelprize~~.~~org/nobel_prizes/medicine/laureates/1963/index~~.~~html~~ | ~~archive~~-~~date~~ = ~~16 July 2007~~ | df = ~~dmy-all~~ }}</~~ref~~> ~~However~~, ~~[[Hodgkin–Huxley model~~|~~their model]] considers only two types~~ of ~~voltage-sensitive ion channels, and makes several assumptions about them, e~~.g.~~, that their internal gates open and close independently of one another~~. ~~In reality, there are many types of ion channels,~~<~~ref name~~=~~"goldin_2007">Goldin~~, AL in ~~{{harvnb~~|~~Waxman~~|~~2007~~|~~loc~~=~~''Neuronal Channels and Receptors'', pp~~. ~~43–58~~.}}</~~ref> and they do not always open and close independently.<ref group="lower-alpha" name=":0"~~>{{cite journal | vauthors = ~~Naundorf B~~, ~~Wolf F, Volgushev M~~ | title = ~~Unique features~~ of ~~action~~ potential ~~initiation~~ in ~~cortical neurons~~ | journal = ~~Nature~~ | volume = ~~440~~ | issue = ~~7087~~ | pages = ~~1060–3~~ | date = April ~~2006~~ | pmid = ~~16625198~~ | doi = 10.~~1038~~/~~nature04610~~ | ~~url~~ = ~~http:~~/~~/www.volgushev.uconn.edu/DownLoads/Naundorf_Nature2006v440p1060_Suppl_3_CoopModel.pdf~~ | df = ~~dmy-all~~ | ~~bibcode~~ = ~~2006Natur~~.~~440~~.~~1060N~~ | ~~s2cid~~ = ~~1328840~~ }}</ref>

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动作电位的过程是由两个耦合的效应决定的。首先，膜电位的变化引起电压敏感离子通道的开关，进而改变了膜对这些离子的渗透性。其次，根据戈德曼方程（[[Goldman equation]]），这种渗透性的变化改变了平衡电位 ''Em''，从而改变了膜电位。<ref name="goldman_1943" group="lower-alpha">{{cite journal | vauthors = Goldman DE | title = Potential, Impedance, and Rectification in Membranes | journal = The Journal of General Physiology | volume = 27 | issue = 1 | pages = 37–60 | date = September 1943 | pmid = 19873371 | pmc = 2142582 | doi = 10.1085/jgp.27.1.37 }}</ref> 因此，膜电位影响渗透性，其又进一步影响膜电位。这就为正反馈（positive feedback）创造了条件，而正反馈正是动作电位上升相的关键。更复杂的是，一个离子通道可能有多个内“门”，对 ''Vm'' 以相反的方式或不同速率做出反应。<ref name="hodgkin_1952" group="lower-alpha">{{cite journal | vauthors = Hodgkin AL, Huxley AF, Katz B | title = Measurement of current-voltage relations in the membrane of the giant axon of Loligo | journal = The Journal of Physiology | volume = 116 | issue = 4 | pages = 424–48 | date = April 1952 | pmid = 14946712 | pmc = 1392219 | doi = 10.1113/jphysiol.1952.sp004716 | author-link1 = Alan Lloyd Hodgkin | author-link3 = Bernard Katz }} * {{cite journal | vauthors = Hodgkin AL, Huxley AF | title = Currents carried by sodium and potassium ions through the membrane of the giant axon of Loligo | journal = The Journal of Physiology | volume = 116 | issue = 4 | pages = 449–72 | date = April 1952 | pmid = 14946713 | pmc = 1392213 | doi = 10.1113/jphysiol.1952.sp004717 | author-link1 = Alan Lloyd Hodgkin }} * {{cite journal | vauthors = Hodgkin AL, Huxley AF | title = The components of membrane conductance in the giant axon of Loligo | journal = The Journal of Physiology | volume = 116 | issue = 4 | pages = 473–96 | date = April 1952 | pmid = 14946714 | pmc = 1392209 | doi = 10.1113/jphysiol.1952.sp004718 | author-link1 = Alan Lloyd Hodgkin }} * {{cite journal | vauthors = Hodgkin AL, Huxley AF | title = The dual effect of membrane potential on sodium conductance in the giant axon of Loligo | journal = The Journal of Physiology | volume = 116 | issue = 4 | pages = 497–506 | date = April 1952 | pmid = 14946715 | pmc = 1392212 | doi = 10.1113/jphysiol.1952.sp004719 | author-link1 = Alan Lloyd Hodgkin }} * {{cite journal | vauthors = Hodgkin AL, Huxley AF | title = A quantitative description of membrane current and its application to conduction and excitation in nerve | journal = The Journal of Physiology | volume = 117 | issue = 4 | pages = 500–44 | date = August 1952 | pmid = 12991237 | pmc = 1392413 | doi = 10.1113/jphysiol.1952.sp004764 | author-link1 = Alan Lloyd Hodgkin }}</ref> 例如，尽管提高 ''Vm'' 能打开电压敏感钠通道中的大多数门，但它也缓慢地关闭通道的“失活门（inactivation gate）”。因此，当 ''Vm'' 突然升高时，钠离子通道一开始打开，然后因较慢的失活而关闭。

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[[Alan Lloyd Hodgkin]] 和 [[Andrew Huxley]] 在 1952 年建立了动作电位各个阶段的电压和电流的精确模型 <ref name="hodgkin_1952" group="lower-alpha" /> ~~并因此在获得~~ 1963 年诺贝尔生理学或医学奖。<ref name="Nobel_1963" group="lower-Greek" /> 然而，他们的模型只考虑了两种类型的电压敏感离子通道，并对其做出几个假设，比如，其内各门的打开和关闭是相互独立的。实际上，离子通道有很多种类型，<ref name="goldin_2007" /> ~~但并不总是独立打开和关闭的。~~<ref name=":0" group="lower-alpha" />

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[[Alan Lloyd Hodgkin]] 和 [[Andrew Huxley]] 在 1952 年建立了动作电位各个阶段的电压和电流的精确模型 <ref name="hodgkin_1952" group="lower-alpha" /> 并因此获得 1963 年诺贝尔生理学或医学奖。<ref name="Nobel_1963" group="lower-Greek">{{cite press release | url = http://nobelprize.org/nobel_prizes/medicine/laureates/1963/index.html | title = The Nobel Prize in Physiology or Medicine 1963 | publisher = The Royal Swedish Academy of Science | year = 1963 | access-date = 2010-02-21 | url-status = live | archive-url = https://web.archive.org/web/20070716195411/http://nobelprize.org/nobel_prizes/medicine/laureates/1963/index.html | archive-date = 16 July 2007 | df = dmy-all }}</ref> 然而，他们的模型只考虑了两种类型的电压敏感性离子通道，并对齐提出几个假定条件，比如，通道内的各门的打开和关闭是相互独立的。实际上，离子通道有很多种类型，<ref name="goldin_2007">Goldin, AL in {{harvnb|Waxman|2007|loc=''Neuronal Channels and Receptors'', pp. 43–58.}}</ref> 且并不总是独立打开和关闭的。<ref name=":0" group="lower-alpha">{{cite journal | vauthors = Naundorf B, Wolf F, Volgushev M | title = Unique features of action potential initiation in cortical neurons | journal = Nature | volume = 440 | issue = 7087 | pages = 1060–3 | date = April 2006 | pmid = 16625198 | doi = 10.1038/nature04610 | url = http://www.volgushev.uconn.edu/DownLoads/Naundorf_Nature2006v440p1060_Suppl_3_CoopModel.pdf | df = dmy-all | bibcode = 2006Natur.440.1060N | s2cid = 1328840 }}</ref>

===刺激和上升相===

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~~A typical action potential begins at the [[axon hillock]]{{sfn|Stevens|1966|p=49}} with a sufficiently strong depolarization, e.g., a stimulus that increases~~ ''Vm''. This depolarization is often caused by the injection of extra sodium [[cation]]s into the cell; these cations can come from a wide variety of sources, such as [[chemical synapse]]s, [[sensory neuron]]s or [[pacemaker potential]]s.

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动作电位通常因刺激提高了 ''Vm'' 等因素使轴丘足够去极化而发生。这种去极化通常是由细胞注入额外的钠离子等阳离子引起的；这些阳离子有多种来源，如化学突触、感觉神经元或起搏电位。

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动作电位通常随着足够的去极化，比如刺激提高了 ''Vm''，而在轴丘发生。这种去极化通常是由细胞注入额外的钠离子等阳离子引起的；这些阳离子有多种来源，如化学突触、感觉神经元或起搏电位。

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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 [[Second law of thermodynamics|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 channel]]s present on the membrane of the neuron causes an [[wikt:Special:Search/efflux|efflux]] of potassium ions making the resting potential close to ''E''K ≈ –75 mV.{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1p=34|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2p=134|3a1=Schmidt-Nielsen|3y=1997|3pp=478–480}} 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.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfn|Junge|1981|pp=89–90}}{{sfn|Schmidt-Nielsen|1997|p=484}} 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.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=48–49|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2p=141|3a1=Schmidt-Nielsen|3y=1997|3p=483|4a1=Junge|4y=1981|4p=89}} A 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 ''E''Na≈ +55 mV. The increasing voltage in turn causes even more sodium channels to open, which pushes ''Vm'' still further towards ''E''Na. This positive feedback continues until the sodium channels are fully open and ''Vm'' is close to ''E''Na.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfn|Junge|1981|pp=89–90}}{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=49–50|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2pp=140–141|3a1=Schmidt-Nielsen|3y=1997|3pp=480–481}}{{sfn|Schmidt-Nielsen|1997|pp=483–484}} The sharp rise in ''Vm'' and sodium permeability correspond to the ''rising phase'' of the action potential.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfn|Junge|1981|pp=89–90}}{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=49–50|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2pp=140–141|3a1=Schmidt-Nielsen|3y=1997|3pp=480–481}}{{sfn|Schmidt-Nielsen|1997|pp=483–484}}

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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，以及静电作用（相反电荷的吸引）是离子进出神经元的原因。由于细胞的 K+ 外流，神经元内部相对于细胞外部带负电。神经细胞膜对 K+ 的渗透性比其他离子更强，使得这种离子能够选择性地顺着浓度梯度流出细胞。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 ''E''K ≈ -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，浓度差和电位差都驱使其进入细胞。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），外向的钾电流大过内向的钠电流，膜复极化回到正常的静息电位 -70 mV 左右。然而，当去极化足够大时，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， ''Vm'' 越是升高，其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'' 接近钠平衡电位 ''E''Na ≈ + 55 mV。电位增加进而导致更多的钠离子通道打开，这使得 ''Vm'' 更靠近 ''E''Na。这种正反馈持续到钠离子通道完全打开，''Vm'' 接近 ''E''Na。''Vm'' 和钠通透性的骤然上升与动作电位的上升相相对应。

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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~~''.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|p=49}}{{sfn|Stevens|1966|pp=19–20}}{{sfnm|1a1=Bullock|1a2=Orkand|1a3=Grinnell|1y=1977|1p=151|2a1=Junge|2y=1981|2pp=4–5}} 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~~''~~.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|p=49}}{{sfn|Stevens|1966|pp=19–20}}{{sfnm|1a1=Bullock|1a2=Orkand|1a3=Grinnell|1y=1977|1p=151|2a1=Junge|2y=1981|2pp=4–5}}~~

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对于处于静息状态的神经元来说，细胞外液的钠离子和氯离子浓度高于细胞内液中，而细胞内液的钾离子浓度高于细胞外液。使离子从高浓度向低浓度移动的浓度差，以及静电作用（相反电荷的吸引）决定离子流出或流入神经元。由于细胞的 K+ 外流，神经元内部相对于外部带负电。神经元的细胞膜对 K+ 的渗透性比其他离子更强，使得这种离子能够选择性地顺着浓度梯度流出细胞。这种浓度梯度以及神经元膜上的钾离子泄漏通道（potassium leak channel）导致钾离子外流，使静息电位接近 ''E''K ≈ -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，浓度差和电位差都驱使其进入细胞。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（比方说，把 ''Vm'' 从 -70 mV 增加到 -60 mV），外向的钾电流大过内向的钠电流，膜复极化回到正常的静息电位 -70 mV 左右。然而，当去极化足够大时，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， ''Vm'' 越是升高，其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'' 趋向钠平衡电位 ''E''Na ≈ +55 mV。电位增加进而导致更多的钠离子通道打开，这使得 ''Vm'' 更趋近 ''E''Na。这种正反馈持续到钠离子通道完全打开，''Vm'' 接近 ''E''Na。''Vm'' 和钠通透性的骤然上升与动作电位的上升相是对应的。

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这种失控状态的临界阈值电位通常在 -45 mV ~~左右，但这取决于轴突最近的活动。一个刚发放了动作电位的细胞不能立即发放新的动作电位，因为~~ Na+ 通道还没有从失活状态恢复过来。不能发放新的动作电位的这段时间叫做绝对不应期（ ''absolute refractory period''~~）。在一些但不是全部的离子通道恢复后，轴突可以被刺激产生新的动作电位，但需要更高的阈值电位，即需要更强的去极化，比如例如~~ -30 ~~mV。动作电位很难引起的阶段称为相对不应期（~~''relative refractory period''）。

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这种失控状态的临界阈值电位通常在 -45 mV 左右，但这取决于轴突最近的活动。刚发放过动作电位的细胞不能立即发放新的动作电位，因为 Na+ 通道还没有从失活状态恢复过来。不能发放新的动作电位的这段时间叫做绝对不应期（''absolute refractory period''）。在部分的离子通道恢复后，轴突可以被刺激产生新的动作电位，但需要更高的阈值电位，即需要更强的去极化，比如 -30 mV。很难触发动作电位的时期称为相对不应期（''relative refractory period''）。

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===~~Peak phase~~ 峰值相===

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===峰值相===

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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 ''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''.{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1p=47|2a1=Purves|2a2=Augustine|2a3=Fitzpatrick|2a4=Hall|2y=2008|2p=65|3a1=Bullock|3a2=Orkand|3a3=Grinnell|3y=1977|3pp=147–148|4a1=Stevens|4y=1966|4p=128}} 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 ''E''K.{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1p=47|2a1=Purves|2a2=Augustine|2a3=Fitzpatrick|2a4=Hall|2y=2008|2p=65|3a1=Bullock|3a2=Orkand|3a3=Grinnell|3y=1977|3pp=147–148|4a1=Stevens|4y=1966|4p=128}} 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.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|p=49}}{{sfn|Bullock|Orkand|Grinnell|1977|p=152}}{{sfn|Schmidt-Nielsen|1997|pp=483–484}}{{sfnm|1a1=Bullock|1a2=Orkand|1a3=Grinnell|1y=1977|1pp=147–149|2a1=Stevens|2y=1966|2pp=126–127}}

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随着钠离子通道最大程度地开放，上升相的正反馈变慢并停止。在动作电位峰值，钠离子的渗透性最大，膜电位 ''Vm'' 几乎等于钠离子的平衡电压 ''E''Na。然而，最初打开钠离子通道的膜电位上升也通过关闭通道孔而慢慢关闭通道；钠离子通道失活。这降低了细胞膜钠离子相对于钾离子的通透性，使膜电位重新回到静息值。同时，膜电位上升打开了电压敏感性钾离子通道，膜的钾离子通透性增加促使 ''Vm'' 向 ''E''K 方向变化。这些钠离子与钾离子的通透性的变化使 ''Vm'' 迅速下降，使膜复极化，产生动作电位的“下降相”。

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~~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~~ ''Vm'' 几乎等于钠离子的平衡电压 ''E''Na。然而，最初打开钠离子通道的升高的电位也会通过关闭它们的孔而慢慢关闭它们；钠离子通道失活。这降低了细胞膜钠离子相对于钾离子的通透性，使膜电位重新回到静息值。同时，升高的膜电位打开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 ''E''K ~~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”。~~

===后超极化===

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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, [[SK channel|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~~ ''E''K. The membrane potential goes below the resting membrane potential. Hence, there is an undershoot or [[hyperpolarization (biology)|hyperpolarization]], termed an [[afterhyperpolarization]], that persists until the membrane potassium permeability returns to its usual value, restoring the membrane potential to the resting state.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|p=37}}{{sfn|Bullock|Orkand|Grinnell|1977|p=152}}

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去极化电位使额外的电压依赖性钾离子通道打开，但当膜恢复至正常的静息电位时，其中一些通道不会立即关闭。此外，在动作电位过程中，钙离子内流会引起更多的钾离子通道打开。细胞内钾离子浓度短暂地变得极低，使膜电位 ''Vm'' 更加接近钾离子平衡电位 ''E''K，甚至低于静息膜电位。因此，存在一个下冲（undershoot）或超极化（hyperpolarization）称为后超极化，持续到膜的钾离子通透性恢复到正常值，恢复膜电位到静息状态。

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去极化电位打开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位时，其中一些通道不会马上关闭。此外，在动作电位过程中，钙离子内流会促使更多的钾离子通道打开。细胞内钾离子浓度短暂地变得极低，使膜电位 ''Vm'' 更加接近钾离子平衡电压 ''E''K，甚至低于静息膜电位。因此，存在一个被称下冲（undershoot）或超极化称为后超极化（ afterhyperpolarization），持续到膜的钾离子通透性恢复到正常值，恢复膜电位到静息状态。

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===不应期===

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===~~不应期Refractory period~~===

Each action potential is followed by a [[refractory period (physiology)|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.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|p=49}}{{sfn|Stevens|1966|pp=19–20}}{{sfnm|1a1=Bullock|1a2=Orkand|1a3=Grinnell|1y=1977|1p=151|2a1=Junge|2y=1981|2pp=4–5}} 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 [[Sodium channel#Gating|"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.

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每个动作电位后面跟着一个不应期，这个不应期可以分为一个绝对不应期，在这个不应期中不可能激发另一个动作电位，然后是一个相对的不应期，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。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，从而导致相对不应期。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，相对的不应期的持续时间是高度可变的。

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每个动作电位后都接着一个不应期，这个不应期可以分绝对不应期和相对不应期。在绝对不应期，完全不能触发另一个动作电位；在随后的相对的不应期，需要异常强的刺激才能引起动作电位。两个不应期是由钠离子和钾离子通道的分子状态变化引起的。在动作电位后关闭的钠通道进入“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。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，从而导致相对不应期。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.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|p=56}} 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.

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绝对不应期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。

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绝对不应期主要负责沿轴突的动作电位的单向传播。在任何特定时刻，活跃发放的位置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。

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==~~Propagation~~==

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==Propagation动作电位的传播==

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

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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。<ref name="Zalc" group="lower-alpha" /><ref name="S. Poliak & E. Peles" group="lower-alpha" /><ref name=":2" group="lower-alpha" /> 髓鞘形成主要存在于脊椎动物中，但是在一些无脊椎动物中也发现了类似的系统，比如某些种类的虾。<ref name=":3" group="lower-alpha" /> 脊椎动物中并不是所有的神经元都是有髓神经元；例如，组成自主神经系统的神经元的轴突一般都不是有髓神经元。

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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~~ [[Metre per second|meter per second]] （m~~/~~s） to over~~ 100~~ ~~m/s~~, and, in general, increases with axonal diameter.~~<ref name="hursh_1939" group=lower-alpha>{{cite journal | vauthors = Hursh JB | year = 1939 | title = Conduction velocity and diameter of nerve fibers | journal = American Journal of Physiology | volume = 127 | pages = 131–39| doi = 10.1152/ajplegacy.1939.127.1.131 }}</ref>

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髓鞘阻止了离子从髓鞘包裹的轴突部位出入。一般地，髓鞘增加了动作电位的传导速度，使其能效更高。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 100 m/s 以上，一般而言，随轴突直径的增大而增大。<ref name="hursh_1939" group="lower-alpha">{{cite journal | vauthors = Hursh JB | year = 1939 | title = Conduction velocity and diameter of nerve fibers | journal = American Journal of Physiology | volume = 127 | pages = 131–39| doi = 10.1152/ajplegacy.1939.127.1.131 }}</ref>

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

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

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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，这足以使郎飞结的第一个或第二个后续节点去极化。相反，郎飞结的一个节点上的动作电位产生的离子电流在下一个节点上激发了另一个动作电位；这种从一个节点到另一个节点的明显的动作电位“跳跃”被称为跳跃式传导。虽然跳跃式传导的机制在1925年由 Ralph Lillie ~~提出,~~<ref name=":4" group="lower-alpha" /> ~~t，但是参见第一个关于跳跃式传导的实验证据来自~~ Ichiji Tasaki ~~Taiji Takeuchi~~ <ref name="tasaki_1939" group="lower-alpha" /> 和 Taiji Takeuchi <ref name="tasaki_1941_1942_1959" group="lower-alpha" /><ref name=":12" /> ~~和来自~~ Andrew Huxley 和 Robert Stämpflii。<ref name="huxley_staempfli_1949_1951" group="lower-alpha" /> 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。

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动作电位不能在有髓鞘的轴突段的膜上传播。不过，电流由细胞质携带的，这足以使后面一两个郎飞结去极化。相反，一个郎飞结的动作电位产生的离子电流在下一个郎飞结引起另一个动作电位；这种从一个结点到另一个结点的动作电位的看似“跳跃”被称为跳跃式传导。虽然跳跃式传导的机制在 1925 年由 Ralph Lillie 提出，<ref name=":4" group="lower-alpha" /> 但是参见第一个关于跳跃式传导的实验证据来自 Ichiji Tasaki <ref name="tasaki_1939" group="lower-alpha" /> 和 Taiji Takeuchi <ref name="tasaki_1941_1942_1959" group="lower-alpha" /><ref name=":12" /> 以及 Andrew Huxley 和 Robert Stämpflii。<ref name="huxley_staempfli_1949_1951" group="lower-alpha" /> 相比之下，在无髓鞘的轴突中，动作电位在紧邻的膜上激发了另一个动作电位，并像波一样不断地沿着轴突移动。

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

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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传至神经肌肉接点引起的，这是神经毒素的一个共同靶点。<ref name="Newmark" group="lower-alpha" />

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===~~植物动作电位Plant action potentials~~===

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===植物动作电位===

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

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

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植物和真菌细胞<ref name="Slayman_1976" group="lower-alpha" /> 也是电兴奋性的。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摄入带正电的钠离子，而是通过释放带负电的氯离子来完成的。<ref name="Mummert_1991" group="lower-alpha" /><ref name="Gradmann_2001" group="lower-alpha" /> 1906 年，J. C. Bose 发表了对先前由 Burdon-Sanderson 和 Darwin 发现的植物动作电位 <ref name=":14" /> 进行了首次测量的结果。细胞质中钙离子的增加可能是阴离子释放进入细胞中的原因。因此，钙可以预测离子运动，比如大麦叶中的负氯离子的内流和正钾离子的外流。<ref name=":15" />

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

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

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

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

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==~~实验方法Experimental methods~~==

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==实验方法==

[[Image:Loligo forbesii.jpg|thumb|right|250px|Giant axons of the longfin inshore squid （''[[Doryteuthis pealeii]]''） were [[Marine Biological Laboratory#Neuroscience, neurobiology, and sensory physiology|crucial for scientists]] to understand the action potential.<ref>{{cite book |url=https://books.google.com/books?id=SDi2BQAAQBAJ |title=The Brain, the Nervous System, and Their Diseases |first=Jennifer L. |last=Hellier | name-list-style = vanc |year=2014 |pages=532 |publisher=ABC-Clio |isbn=9781610693387}}</ref>长鳍近海鱿鱼（Doryteuthis pealeii）的巨型轴突对于科学家了解动作电位至关重要。[注1]|链接=Special:FilePath/Loligo_forbesii.jpg]]

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第三个问题是如何获得足够小的电极来记录单个轴突内的电压而不对其造成干扰，这个问题在1949年由于玻璃微移液管电极，<ref name="ling_1949" group="lower-alpha" /> 的发明而得到解决，并且很快被其他研究人员采用。<ref name="nastuk_1950" group="lower-alpha" /><ref name="brock_1952" group="lower-alpha" /> 这种方法的改进可以生产出100纳米的电极尖端，同时也提供了高的输入阻抗。<ref name=":20" /> 动作电位中的 Snell 和 FM 也可以用放置在神经元旁的小金属电极记录下来，用含有th [[neurochip]]s containing [[EOSFET]]s eosfet 的神经芯片，或者用对 Ca2+ 或电压敏感的染料记录下来。<ref name="dyes" group="lower-alpha" />

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

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

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

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~~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 [[Erwin Neher~~]] and [[Bert Sakmann]].埃尔温 · 内尔和伯特 · 萨克曼发明的膜片钳（patch clamp）成为可能。由于这一发现，他们在1991年被授予诺贝尔生理学或医学奖科学奖。<ref name="Nobel_1991" group="lower-Greek" /> 膜片钳技术证实了离子通道具有分立的电导状态，如开放状态、闭合状态和失活状态。

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电压钳电极揭示了，离子通道有两个状态：开放（高电导）和关闭（低电导）。|链接=Special:FilePath/Single_channel.png]]

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[[~~Optical imaging~~]] ~~technologies have been developed in recent years to measure action potentials, either via simultaneous multisite recordings or with ultra-spatial resolution. Using~~ [[~~Potentiometric dyes|voltage-sensitive dyes~~]]~~, action potentials have been optically recorded from a tiny patch of [[cardiomyocyte]] membrane.~~<ref name="~~pmid19289075~~" group="lower-~~alpha~~">{{cite ~~journal~~ | ~~vauthors~~ = ~~Bu G, Adams H, Berbari EJ, Rubart M~~ | title = ~~Uniform action potential repolarization within the sarcolemma of~~ in ~~situ ventricular cardiomyocytes~~ | ~~journal~~ = ~~Biophysical Journal~~ | ~~volume~~ = ~~96 | issue = 6 | pages = 2532–46~~ | date = ~~March 2009~~ | ~~pmid~~ = ~~19289075~~ | ~~pmc~~ = ~~2907679 | doi = 10.1016~~/j.~~bpj~~.~~2008~~.12.~~3896~~ | ~~bibcode~~ = ~~2009BpJ....96.2532B~~ }}</ref>

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玻璃微电极测量的是很多离子通道的总电流，在 1970 年代 [[Erwin Neher]] 和 [[Bert Sakmann]] 发明的膜片钳（patch clamp）使研究单个离子通道的电学性质成为可能。两位科学家因此被授予 1991 年诺贝尔生理学或医学奖科学奖。<ref name="Nobel_1991" group="lower-Greek">{{cite press release | url = http://nobelprize.org/nobel_prizes/medicine/laureates/1991/press.html | title = The Nobel Prize in Physiology or Medicine 1991 | publisher = The Royal Swedish Academy of Science | year = 1991 | access-date = 2010-02-21 | url-status = live | archive-url = https://web.archive.org/web/20100324031907/http://nobelprize.org/nobel_prizes/medicine/laureates/1991/press.html | archive-date = 24 March 2010 | df = dmy-all }}</ref> 膜片钳技术证实了离子通道具有分立的电导状态，如打开状态、关闭状态和失活状态。

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~~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。~~<ref name="pmid19289075" group="lower-alpha" />

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近年来发展了光学成像（optical imaging）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（voltage-sensitive dyes），可以光学记录小块心肌细胞（cardiomyocyte）膜的动作电位。<ref name="pmid19289075" group="lower-alpha">{{cite journal | vauthors = Bu G, Adams H, Berbari EJ, Rubart M | title = Uniform action potential repolarization within the sarcolemma of in situ ventricular cardiomyocytes | journal = Biophysical Journal | volume = 96 | issue = 6 | pages = 2532–46 | date = March 2009 | pmid = 19289075 | pmc = 2907679 | doi = 10.1016/j.bpj.2008.12.3896 | bibcode = 2009BpJ....96.2532B }}</ref>

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==~~神经毒素Neurotoxins~~==

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==神经毒素==

[[Image:Puffer Fish DSC01257.JPG|thumb|right|[[Tetrodotoxin]] is a lethal toxin found in [[pufferfish]] that inhibits the [[voltage-gated ion channel|voltage-sensitive sodium channel]], halting action potentials.|链接=Special:FilePath/Puffer_Fish_DSC01257.JPG]]

Several [[neurotoxin]]s, 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 "[[Paralytic shellfish poisoning|red tide]]s"） block action potentials by inhibiting the voltage-sensitive sodium channel;<ref name="TTX_refs" group="lower-alpha">{{cite journal | vauthors = Milligan JV, Edwards C | title = Some factors affecting the time course of the recovery of contracture ability following a potassium contracture in frog striated muscle | journal = The Journal of General Physiology | volume = 48 | issue = 6 | pages = 975–83 | date = July 1965 | pmid = 5855511 | pmc = 2195447 | doi = 10.1085/jgp.48.6.975 }} * {{cite book | vauthors = Ritchie JM, Rogart RB | title = Reviews of Physiology, Biochemistry and Pharmacology, Volume 79 | chapter = The binding of saxitoxin and tetrodotoxin to excitable tissue | volume = 79 | pages = 1–50 | year = 1977 | pmid = 335473 | doi = 10.1007/BFb0037088 | isbn = 0-387-08326-X | series = Reviews of Physiology, Biochemistry and Pharmacology }} * {{cite journal | vauthors = Keynes RD, Ritchie JM | title = On the binding of labelled saxitoxin to the squid giant axon | journal = Proceedings of the Royal Society of London. Series B, Biological Sciences | volume = 222 | issue = 1227 | pages = 147–53 | date = August 1984 | pmid = 6148754 | doi = 10.1098/rspb.1984.0055 | bibcode = 1984RSPSB.222..147K | s2cid = 11465181 }}</ref> similarly, [[dendrotoxin]] from the [[mamba|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 warfare|chemical weapon]]s. Neurotoxins aimed at the ion channels of insects have been effective [[insecticide]]s; 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.

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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。

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一些天然和人造的神经毒素（neurotoxins）被设计用来阻断动作电位。来自河豚（pufferfish）的河豚毒素（tetrodotoxin）和来自沟鞭藻属（Gonyaulax）的石房蛤毒素（saxitoxin）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（[[mamba|black mamba]]）蛇的树眼镜蛇毒素（dendrotoxin）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（affinity chromatography）来纯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（permethrin），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==

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

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

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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励了Alessandro Volta 发明了伏打电堆（voltaic pile）ーー已知最早的电池ーー他用这种电池研究了动物电（如电鳗）以及对直流电压的生理反应。<ref name="piccolino_2000" group="lower-alpha" />

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

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

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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）。Carlo Matteucci 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。[[Carlo Matteucci]] 的工作启发了德国生理学家 [[Emil du Bois-Reymond]]，后者在1843 年发现了动作电位.<ref name=":21" /> 。动作电位的传导速度最早是在1850年由du Bois-Reymond 杜波依斯-雷蒙德的朋友[[Hermann von Helmholtz]]赫尔曼·冯·亥姆霍兹 · 雷蒙德测量的.<ref name=":22" /> 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 [[Santiago Ramón y Cajal]] 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，Golgi 和 [[Santiago Ramón y Cajal|Ramón y Cajal]] 获得了1906年的诺贝尔生理学奖.<ref name="Nobel_1906" group="lower-Greek" /> 。他们的工作解决了19世纪神经解剖学中长期存在的争议；高尔基自己则主张神经系统的网络模型。

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

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

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

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

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

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

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

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==~~定量模型Quantitative models~~==

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==定量模型==

[[Image:MembraneCircuit.svg|thumb|336px|right|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 [[electrical conductance|conductances]] of four types of ions. The two conductances on the left, for potassium （K） and sodium （Na）, are shown with arrows to indicate that they can vary with the applied voltage, corresponding to the [[voltage-gated ion channel|voltage-sensitive ion channels]]. The two conductances on the right help determine the [[resting membrane potential]].

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

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

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

==Notes==

Okxy

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个编辑