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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。

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

在神经元中，动作电位在细胞与细胞之间的通讯中起着中心作用，它可以以跳跃式传导（saltatory conduction ）方式，协助神经信号沿着轴突向位于轴突末端的突触结传播；然后信号通过突触传递到其他神经元、运动细胞或腺体。在其他类型的细胞中，它们的主要功能是激活细胞内的反应过程。例如，在肌肉细胞中，动作电位是引起肌肉收缩的一系列事件的第一步。在胰腺的 β 细胞中，它们会刺激胰岛素的释放<ref name="pmid16464129" group="lower-alpha">{{cite journal | vauthors = MacDonald PE, Rorsman P | title = Oscillations, intercellular coupling, and insulin secretion in pancreatic beta cells | journal = PLOS Biology | volume = 4 | issue = 2 | pages = e49 | date = February 2006 | pmid = 16464129 | pmc = 1363709 | doi = 10.1371/journal.pbio.0040049 }} {{open access}}</ref>。神经元的动作电位也被称为“神经冲动（neural impulse）”或“脉冲（spike）”，神经元产生的动作电位的时间序列被称为“动作电位序列（spike train）”。神经元发出动作电位或神经冲动，也常说神经在“发放（fire）”。

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）”。

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

动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）。

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

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

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

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

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

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

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

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

神经元是电兴奋型细胞，一般包含一个或多个树突、一个胞体、一个轴突以及一个或多个轴突末梢。树突是细胞的突起，其主要功能是接收突触信号。突触上的突起被称为树突棘，用来捕获突触前神经元释放的神经递质。其上分布有高密度的配体门控离子通道。这些棘有一个细细的颈部，连接球状突起和树突。这确保树突棘内部发生的变化不太可能影响邻近的树突棘。树突棘除了极少数例外情况（见 LTP），可以作为一个独立的单位工作。树突从胞体延伸出来，胞体是细胞核和许多“正常”的真核细胞器的所在。与树突棘不同，胞体的表面布满了电压可激活的离子通道。这些通道帮助传输由树突产生的信号。从胞体延伸出来的是轴丘。这个区域的特征是有非常高浓度的电压激活钠离子通道。一般认为它是动作电位的起始区，或触发区。在树突棘处产生的多个信号，经胞体传输而汇聚于此。轴丘之后便是轴突。这是一个从胞体中延伸出来的细管状突起。轴突被髓鞘（myelin）绝缘。髓鞘由神经胶质细胞组成，在外周神经系统是施万细胞，在中央神经系统为少突胶质细胞。虽然神经胶质细胞不参与电信号的传递，但可以与神经元通讯和提供重要的生化支持。具体来说，髓鞘绕着轴突多重包裹，形成一层厚厚的脂肪层，阻止离子进入或逃离轴突。这种绝缘可以避免信号发生剧烈的衰减，并确保信号更快速地传播；但同时会限制轴突表面，使其没有离子通道。因此，在轴突上每隔一段就会有块不带绝缘层的膜片。这些郎飞结（nodes of Ranvier）可以被认为是“迷你轴丘”，因为其目的是增强信号，以避免明显的信号衰减。在最远端，轴突失去绝缘的髓鞘，并开始分支成几个轴突末梢。这些突触前末梢，或称突触结（synaptic bouton），是突触前细胞轴突内的一个特殊区域，其中包含神经递质，这些神经递质被包装在称为突触小泡的膜包裹的小球内。

神经元是电兴奋型细胞，一般包含一个或多个树突、一个胞体、一个轴突以及一个或多个轴突末梢。树突是细胞的突起，其主要功能是接收突触信号。突触上的突起被称为树突棘，用来捕获突触前神经元释放的神经递质。其上分布有高密度的配体门控离子通道。这些棘有一个细细的颈部，连接球状突起和树突。这确保树突棘内部发生的变化不太可能影响邻近的树突棘。树突棘除了极少数例外情况（见 LTP），可以作为一个独立的单位工作。树突从胞体延伸出来，胞体是细胞核和许多“正常”的真核细胞器的所在。与树突棘不同，胞体的表面布满了电压可激活的离子通道。这些通道帮助传输由树突产生的信号。从胞体延伸出来的是轴丘。这个区域的特征是有非常高浓度的电压激活钠离子通道。一般认为它是动作电位的起始区，或触发区。在树突棘处产生的多个信号，经胞体传输而汇聚于此。轴丘之后便是轴突。这是一个从胞体中延伸出来的细管状突起。轴突被髓鞘（myelin）绝缘。髓鞘由神经胶质细胞组成，在外周神经系统是施万细胞，在中央神经系统为少突胶质细胞。虽然神经胶质细胞不参与电信号的传递，但可以与神经元通讯和提供重要的生化支持。具体来说，髓鞘绕着轴突多重包裹，形成一层厚厚的脂肪层，阻止离子进入或逃离轴突。这种绝缘可以避免信号发生剧烈的衰减，并确保信号更快速地传播；但同时会限制轴突表面，使其没有离子通道。因此，在轴突上每隔一段就会有块不带绝缘层的膜片。这些郎飞结（nodes of Ranvier）可以被认为是“迷你轴丘”，因为其目的是增强信号，以避免明显的信号衰减。在最远端，轴突失去绝缘的髓鞘，并开始分支成几个轴突末梢。这些突触前末梢，或称突触扣结，是突触前细胞轴突内的一个特殊区域，其中包含神经递质，这些神经递质被包装在称为突触小泡的膜包裹的小球内。

===动作电位的触发===

===动作电位的触发===

[[Image:SynapseSchematic en.svg|thumb|right|300px|当动作电位传至突触前轴突末端（上部）时，它会导致神经递质分子的释放，这些分子打开突触后神经元中的离子通道（底部）。输入引起的兴奋性和抑制性突触后电位在突触后神经元中整合引起新的动作电位。|链接=Special:FilePath/SynapseSchematic_en.svg]]

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

 

===动作电位的动力学===

===动作电位的动力学===

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.

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.

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}}

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}}

 

动作电位的幅度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" /><ref name="Aur" group="lower-alpha" /><ref name="Aur, Jog" group="lower-alpha" /> 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。

===Sensory neurons 感觉神经元===

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===

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]].

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]].

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。

 

[[文件:Pacemaker potential.svg.png|替代=|缩略图|In [[pacemaker potential]]s, the cell spontaneously depolarizes （straight line with upward slope） until it fires an action potential.

在起搏电位中，细胞自发地去极化（具有向上斜率的直线），直到它发放动作电位。]]

[[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。]]

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]].

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

在感觉神经元中，动作电位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。心脏窦房结的心律起搏细胞就是一个很好的例子。<ref name="noble_1960" group="lower-alpha" /> 虽然这种起搏电位具有自然节律，但它可以通过外部刺激进行调节；例如，药物以及交感神经和副交感神经发出的信号可以改变心率。外部刺激不会引起细胞的反复放电，只是改变了它的放电频率。在某些情况下，频率的调节可能更加复杂，引致动作电位的特定发放模式，如爆发（bursting）。

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）。

==Phases 动作电位的相位==

==动作电位的相位==

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}}

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}}

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

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

动作电位的过程是由两个耦合的效应决定的。首先，膜电位的变化引起电压敏感离子通道的打开和关闭，进而改变了膜对这些离子的渗透性。其次，根据戈德曼方程，这种渗透率的变化改变了平衡电位 Em，从而改变了膜电位.<ref name="goldman_1943" group="lower-alpha" /> T。因此，膜电位影响渗透性，进而进一步影响膜电位。这就为正反馈提供了可能性，而正反馈是动作电位上升相的关键。令事情更复杂的是，一个离子通道可能有多个内部“门”，对 ''V_m'' i以相反的或不同的速率的反应。<ref name="hodgkin_1952" group="lower-alpha" /> 例如，尽管提高 ''V_m'' 可以打开电压敏感钠通道中的大多数门，但它也可以关闭通道的“失活门”，尽管速度更慢。因此，当 Vm 突然升高时，钠离子通道开始打开，但随后随着较慢的失活而关闭。

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 ''E_m''，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 ''V_m'' 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 ''V_m'' 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  ''V_m'' 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。

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>

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

艾伦·劳埃德·霍奇金和 Andrew Huxley 在1952年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1963年获得了诺贝尔生理学或医学奖动作电位奖。<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，并对它们做出了几个假设，例如，它们的内部门的开启和关闭是相互独立的。实际上，离子通道有很多种类型，<ref name="goldin_2007" /> 它们并不总是独立开启和关闭的。<ref name=":0" group="lower-alpha" />

[[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" />

===Stimulation and rising phase 刺激和上升期===

===刺激和上升相===

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 ''V_m''. 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.

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 ''V_m''. 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.

动作电位通常随着足够的去极化，比如刺激提高了 ''V_m''，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。

 

典型的动作电位因足够的去极化，比如刺激提高了 ''V_m''，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。

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&nbsp;≈&nbsp;–75&nbsp;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 ''V_m'' from −70&nbsp;mV to −60&nbsp;mV）, the outward potassium current overwhelms the inward sodium current and the membrane repolarizes back to its normal resting potential around −70&nbsp;mV.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfn|Junge|1981|pp=89–90}}{{sfn|Schmidt-Nielsen|1997|p=484}} However, if the depolarization is large enough, the inward sodium current increases more than the outward potassium current and a runaway condition （[[positive feedback]]） results: the more inward current there is, the more ''V_m'' increases, which in turn further increases the inward current.{{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 ''V_m''） causes the voltage-sensitive sodium channels to open; the increasing permeability to sodium drives ''V_m'' closer to the sodium equilibrium voltage ''E''_Na≈ +55&nbsp;mV. The increasing voltage in turn causes even more sodium channels to open, which pushes ''V_m'' still further towards ''E''_Na. This positive feedback continues until the sodium channels are fully open and ''V_m'' is close to ''E''_Na.{{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 ''V_m'' 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}}

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&nbsp;≈&nbsp;–75&nbsp;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 ''V_m'' from −70&nbsp;mV to −60&nbsp;mV）, the outward potassium current overwhelms the inward sodium current and the membrane repolarizes back to its normal resting potential around −70&nbsp;mV.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfn|Junge|1981|pp=89–90}}{{sfn|Schmidt-Nielsen|1997|p=484}} However, if the depolarization is large enough, the inward sodium current increases more than the outward potassium current and a runaway condition （[[positive feedback]]） results: the more inward current there is, the more ''V_m'' increases, which in turn further increases the inward current.{{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 ''V_m''） causes the voltage-sensitive sodium channels to open; the increasing permeability to sodium drives ''V_m'' closer to the sodium equilibrium voltage ''E''_Na≈ +55&nbsp;mV. The increasing voltage in turn causes even more sodium channels to open, which pushes ''V_m'' still further towards ''E''_Na. This positive feedback continues until the sodium channels are fully open and ''V_m'' is close to ''E''_Na.{{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 ''V_m'' 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}}

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。神经元内部相对于细胞外部带负电，来自于细胞的 K⁺ 外流。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&nbsp;≈&nbsp;-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它们进入细胞。去极化打开了细胞膜上的钠通道和钾通道，允许离子分别流入和流出轴突。如果去极化很小（比如说，把 ''V_m'' 从 -70 mV 增加到 -60 mV），外向的钾电流压倒内向的钠电流，膜在 -70 mV 左右复极化恢复到正常的静息电位。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，内向钠电流越大，反过来又进一步增加内向钠电流。足够强的去极化（ ''V_m'' 的增加）使电压敏感的钠通道开放，钠的渗透性增加使  ''V_m'' 接近钠平衡电压 ''E''_Na ≈ + 55 mV。增加的电压依次导致更多的钠离子通道打开，这使得 ''V_m''  更靠近 ''E''_Na。这种正反馈持续到钠离子通道完全打开， ''V_m'' 接近 ENa。 ''V_m'' 和钠通透性的急剧升高与动作电位的升高相对应。

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&nbsp;≈&nbsp;-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 ''V_m'' 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， ''V_m'' 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（ ''V_m'' 的增加）使电压敏感的钠通道开放，钠的渗透性增加使  ''V_m'' 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 ''V_m''  更靠近 ''E''_Na。这种正反馈持续到钠离子通道完全打开，''V_m'' 接近 ''E''_Na。''V_m'' 和钠通透性的骤然上升与动作电位的上升相相对应。

The critical threshold voltage for this runaway condition is usually around −45&nbsp;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&nbsp;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}}

The critical threshold voltage for this runaway condition is usually around −45&nbsp;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&nbsp;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}}

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。一个刚刚激发了动作电位的细胞不能立即激发另一个动作电位，因为 Na + 通道还没有从失活状态恢复过来。没有新的动作电位被激发的这段时间叫做绝对不应期。在更长的时间里，当一些但不是全部的离子通道恢复后，轴突可以被刺激产生另一个动作电位，但是具有更高的阈值，需要更强的去极化，例如-30mv。动作电位很难唤起的阶段称为相对不应期。

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''）。

===Peak phase 峰值相===

===Peak phase 峰值相===

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

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

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

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

===髓鞘和跳跃式传导Myelin and saltatory conduction===

===髓鞘和跳跃式传导Myelin and saltatory conduction===