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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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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）”。

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

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

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==神经传递==

===神经元的解剖学===

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

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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。

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

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动作电位沿轴突的传播并止于突触结之前，要先在轴丘触发。基本的触发条件就是把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。

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动作电位沿轴突传播并终于突触结之前，要先在轴丘触发。基本的触发条件就是把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===

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

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动作电位通常由突触前神经元引起的的兴奋性突触后电位引起。通常，神经递质分子由突触前神经元释放后，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。无论膜电位是升高还是降低，这种变化都会被动地传播到膜的邻近区域（如电缆方程及其改进所描述的）。通常情况下，电位刺激随着突触的距离和神经递质结合的时间成指数衰减。兴奋性电位一部分可能到达轴丘，并且（在少数情况下）使膜去极化，足以引起新的动作电位。更典型的是，来自几个突触的兴奋性电位必须在几乎同一时间共同刺激引起新的动作电位。他们的共同作用，当然也可能被反作用的抑制性突触后电位所阻遏。

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}}

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

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神经传导也可以通过电突触发生。通过兴奋性细胞之间以缝隙连接的形式的直接联系，动作电位可以从一个细胞直接传递到下一个细胞。离子在细胞之间的自由流动使得非化学介导的快速传输成为可能。整流通道确保动作电位通过电突触单向移动。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。

==="All-or-none" principle“全或无”原理===

The [[amplitude]] of an action potential is independent of the amount of current that produced it. In other words, larger currents do not create larger action potentials. Therefore, action potentials are said to be [[All-or-none law|all-or-none]] signals, since either they occur fully or they do not occur at all.<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> This is in contrast to [[receptor potential]]s, whose amplitudes are dependent on the intensity of a stimulus.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|pp=26–28}} In both cases, the [[frequency]] of action potentials is correlated with the intensity of a stimulus.

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动作电位的幅度与产生动作电位的电流量无关。换句话说，更大的电流不会产生更大的动作电位。因此，动作电位被称为全或无信号，因为它们要么完全发生，要么根本不发生。<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。在这两种情况下，动作电位的频率都与刺激的强度相关。~~

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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===

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

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在感觉神经元中，外部信号如压力、温度、光或声音与离子通道的开启和关闭相耦合，进而又改变了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），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一定程度，以激发动作电位。人类的一些例子包括嗅觉受器神经元和迈斯纳氏小体（），它们分别对嗅觉和触觉至关重要。然而，并不是所有的感觉神经元都将外部信号转换成动作电位，有些甚至没有轴突。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的开关，这可能导致神经递质分子的释放。同样，在人类视网膜中，第一层的光敏感的感光细胞和下一层的细胞（包括双极细胞和水平细胞）不产生动作电位，只有一些无长突细胞和第三层的神经节细胞产生动作电位，并沿视神经传递。

===Pacemaker potentials 起搏电位===

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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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在感觉神经元中，动作电位来自外部刺激。然而，一些兴奋型细胞不需要这样的刺激就可以发放动作电位：它们自发地使轴丘去极化，并以一个规律的速率发放动作电位，就像一个内部时钟。这种细胞的电压描记称为起搏电位。心脏窦房结的心律起搏细胞就是一个很好的例子。<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，导致动作电位的发放模式，如爆发。

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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。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）。

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==Phases==

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==Phases 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}}

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

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动作电位的过程可分为五部分：上升相、峰值相、下降相、下冲相和不应期。在上升相，膜电位去极化（变得更加积极）。退极化停止的点称为峰值相位。在这个阶段，膜电位达到了最大值。在这之后，有一个下降的阶段。在这个阶段，膜电位变得更负，回到了静息电位。下极化或后超极化阶段是膜电位暂时变得比静止时更加负极化的时期（超极化）。最后，不可能或难以触发随后的动作电位的时间被称为不应期，它可能与其他阶段重叠。

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阶段的关键部分。一个复杂的因素是，单个离子通道可能有多个内部“门”，以相反的方式或不同的速率响应 Vm 中的变化.{{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" /> F<~~ref name="hodgkin_1952" group="lower-alpha"~~ />~~。例如，尽管提高 Vm~~ 可以打开电压敏感钠通道中的大多数门，但它也可以关闭通道的“失活门”，尽管速度更慢。因此，当 Vm 突然升高时，钠离子通道开始打开，但随后随着较慢的失活而关闭。

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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 ''Vm'' 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 ''Vm'' 可以打开电压敏感钠通道中的大多数门，但它也可以关闭通道的“失活门”，尽管速度更慢。因此，当 Vm 突然升高时，钠离子通道开始打开，但随后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>

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艾伦·劳埃德·霍奇金和 Andrew Huxley ~~在1952年精确地模拟了动作电位各个阶段的电压和电流,~~<ref name="hodgkin_1952" group="lower-alpha" /> ~~f。，并因此在1963年获得了诺贝尔生理学或医学奖动作电位奖523.~~<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" />

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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" />

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

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<nowiki>= = = 刺激和上升期 = = =</nowiki>

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

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典型的动作电位因足够的去极化，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。

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

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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。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 ≈ -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 ''Vm'' 从 -70 mV 增加到 -60 mV），外向的钾电流压倒内向的钠电流，膜在 -70 mV 左右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（ ''Vm'' 的增加）使电压敏感的钠通道开放，钠的渗透性增加使 ''Vm'' 接近钠平衡电压 ''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 ''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 ENa。 ''Vm'' 和钠通透性的急剧升高与动作电位的升高相对应。

The critical threshold voltage for this runaway condition is usually around −45 mV, but it depends on the recent activity of the axon. A cell that has just fired an action potential cannot fire another one immediately, since the Na+ channels have not recovered from the inactivated state. The period during which no new action potential can be fired is called the ''absolute refractory period''.{{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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~~这种失控状态的关键阈值电压通常在~~ -45 mV 左右，但这取决于轴突最近的活动。一个刚刚激发了动作电位的细胞不能立即激发另一个动作电位，因为 Na + 通道还没有从失活状态恢复过来。没有新的动作电位被激发的这段时间叫做绝对不应期（性）。在更长的时间里，当一些但不是全部的离子通道恢复后，轴突可以被刺激产生另一个动作电位，但是具有更高的阈值，需要更强的去极化，例如-~~30mv。动作电位异常难以唤起的时期称为相对不应期（性）。~~

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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。

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===Peak phase===

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===Peak phase 峰值相===

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

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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===

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。细胞内钾离子浓度瞬时变得极低，使膜电位 ''Vm'' 更加接近钾离子平衡电压 ''E''K。膜电位会低于静息膜电位。因此，存在一个被称负冲（undershoot）或超极化称为后超极化（ afterhyperpolarization），持续到膜钾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。

===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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~~<nowiki>= = =</nowiki>~~

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

The absolute refractory period is largely responsible for the unidirectional propagation of action potentials along axons.{{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（性）主要负责沿轴突的动作电位的单向传播。在任何特定的时刻，活跃刺激部位后面的一小块轴突是不应激的，但是前面的一小块最近没有被激活，能够被动作电位的去极化刺激。

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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。

==Propagation==

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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轴突柄处产生的动作电位沿轴突传播。当动作电位沿轴突扩散时，电流在轴突上的某一点向内流动，并使其膜的相邻部分去极化。如果足够强的话，这种去极化会在相邻的膜片上激发类似的动作电位。这一基本机制在1937年由艾伦·劳埃德·霍奇金证明。在挤压或冷却神经节段，从而阻断动作电位后，他表明，动作电位到达阻滞的一侧可以激发另一侧的动作电位，只要阻滞的节段足够短。rt.<ref name=":1" group="lower-alpha" /> *

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轴丘产生的动作电位沿轴突传播。当动作电位沿轴突扩散时，电流在轴突上的某一点向内流动，并使其膜的相邻部分去极化。如果足够强的话，这种去极化会在相邻的膜片上激发类似的动作电位。这一基本机制在1937年由艾伦·劳埃德·霍奇金 Alan Lloyd Hodgkin 证明。在挤压或冷却神经节段，从而阻断动作电位后，他表明，动作电位到达阻滞的一侧可以激发另一侧的动作电位，只要阻滞的节段足够短。<ref name=":1" group="lower-alpha" />

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.

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

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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。

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

In order to enable fast and efficient transduction of electrical signals in the nervous system, certain neuronal axons are covered with [[myelin]] sheaths. Myelin is a multilamellar membrane that enwraps the axon in segments separated by intervals known as [[nodes of Ranvier]]. It is produced by specialized cells: [[Schwann cell]]s exclusively in the [[peripheral nervous system]], and [[oligodendrocyte]]s exclusively in the [[central nervous system]]. Myelin sheath reduces membrane capacitance and increases membrane resistance in the inter-node intervals, thus allowing a fast, saltatory movement of action potentials from node to node.<ref name=Zalc group=lower-alpha>{{cite journal | vauthors = Zalc B | title = The acquisition of myelin: a success story | journal = Novartis Foundation Symposium | volume = 276 | pages = 15–21; discussion 21–5, 54–7, 275–81 | year = 2006 | pmid = 16805421 | doi = 10.1002/9780470032244.ch3 | isbn = 978-0-470-03224-4 | series = Novartis Foundation Symposia }}</ref><ref name="S. Poliak & E. Peles" group=lower-alpha>{{cite journal | vauthors = Poliak S, Peles E | title = The local differentiation of myelinated axons at nodes of Ranvier | journal = Nature Reviews. Neuroscience | volume = 4 | issue = 12 | pages = 968–80 | date = December 2003 | pmid = 14682359 | doi = 10.1038/nrn1253 | s2cid = 14720760 }}</ref><ref group="lower-alpha" name=":2">{{cite journal | vauthors = Simons M, Trotter J | title = Wrapping it up: the cell biology of myelination | journal = Current Opinion in Neurobiology | volume = 17 | issue = 5 | pages = 533–40 | date = October 2007 | pmid = 17923405 | doi = 10.1016/j.conb.2007.08.003 | s2cid = 45470194 }}</ref> Myelination is found mainly in [[vertebrate]]s, but an analogous system has been discovered in a few invertebrates, such as some species of [[shrimp]].<ref group="lower-alpha" name=":3">{{cite journal | vauthors = Xu K, Terakawa S | title = Fenestration nodes and the wide submyelinic space form the basis for the unusually fast impulse conduction of shrimp myelinated axons | journal = The Journal of Experimental Biology | volume = 202 | issue = Pt 15 | pages = 1979–89 | date = August 1999 | doi = 10.1242/jeb.202.15.1979 | pmid = 10395528 | url = http://jeb.biologists.org/cgi/pmidlookup?view=long&pmid=10395528 }}</ref> Not all neurons in vertebrates are myelinated; for example, axons of the neurons comprising the autonomous nervous system are not, in general, myelinated.

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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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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。

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

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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，这足以使兰花的第一个或第二个后续节点去极化。相反，Ranvier 的一个节点上的动作电位产生的离子电流在下一个节点上激发了另一个动作电位; 这种从一个节点到另一个节点的明显的动作电位“跳跃”被称为跳跃式传导。虽然跳跃式传导的机制在1925年由 Ralph Lillie 提出,<ref name=":4" group="lower-alpha" /> t，但是参见第一个关于跳跃式传导的实验证据来自 Ichiji Tasaki 和 Taiji Takeuchi <ref name="tasaki_1939" group="lower-alpha" />~~ Tasaki，i~~<ref name="tasaki_1941_1942_1959" group="lower-alpha" /><ref name=":12" /> ~~ani in~~ 和来自 Andrew Huxley 和 Robert ~~Stämpflii.~~<ref name="huxley_staempfli_1949_1951" group="lower-alpha" /> ~~B。相比之下，在无髓鞘的轴突中，动作电位在紧邻的膜上激发了另一个动作电位，并像波一样不断地沿着轴突移动。~~

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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。

[[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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Myelin has two important advantages: fast conduction speed and energy efficiency. For axons larger than a minimum diameter （roughly 1 [[micrometre]]）, myelination increases the [[conduction velocity]] of an action potential, typically tenfold.<ref name="hartline_2007" group=lower-alpha /> Conversely, for a given conduction velocity, myelinated fibers are smaller than their unmyelinated counterparts. For example, action potentials move at roughly the same speed （25 m/s） in a myelinated frog axon and an unmyelinated [[squid giant axon]], but the frog axon has a roughly 30-fold smaller diameter and 1000-fold smaller cross-sectional area. Also, since the ionic currents are confined to the nodes of Ranvier, far fewer ions "leak" across the membrane, saving metabolic energy. This saving is a significant [[natural selection|selective advantage]], since the human nervous system uses approximately 20% of the body's metabolic energy.<ref name="hartline_2007" group=lower-alpha>{{cite journal | vauthors = Hartline DK, Colman DR | title = Rapid conduction and the evolution of giant axons and myelinated fibers | journal = Current Biology | volume = 17 | issue = 1 | pages = R29-35 | date = January 2007 | pmid = 17208176 | doi = 10.1016/j.cub.2006.11.042 | s2cid = 10033356 | doi-access = free }}</ref>

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髓鞘具有两个重要的优点: 传导速度快和能量效率高。对于大于最小直径（大约1微米）的轴突，髓鞘形成增加了动作电位的传导速度，通常是原来的十倍.<ref name="hartline_2007" group="lower-alpha" /> ~~Co。相反，对于一定的传导速度，有髓纤维比无髓纤维小。例如，在有髓青蛙轴突和无髓青蛙轴突中，动作电位的移动速度大致相同（25米~~/秒），但是青蛙轴突的直径要小30倍，横截面积要小1000倍。此外，由于离子电流仅限于郎飞结，跨膜“泄漏”的离子要少得多，从而节省了新陈代谢能量。这种节省是一个重大的选择优势，因为人类神经系统消耗大约20% 的身体代谢能量.<ref name="hartline_2007" group="lower-alpha" />。

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髓鞘具有两个重要的优点：传导速度快和能量效率高。对于大于最小直径（大约1微米）的轴突，髓鞘形成增加了动作电位的传导速度，通常是原来的十倍.<ref name="hartline_2007" group="lower-alpha" /> Co。相反，相同的传导速度，有髓纤维比无髓纤维小。例如，在有髓青蛙轴突和无髓青蛙轴突中，动作电位的移动速度大致相同（25米/秒），但是青蛙轴突的直径要小30倍，横截面积要小1000倍。此外，由于离子电流仅限于郎飞结，跨膜“泄漏”的离子要少得多，从而节省了新陈代谢能量。这种节省是一个重大的选择优势，考虑到人类神经系统消耗大约20% 的身体代谢能量.<ref name="hartline_2007" group="lower-alpha" />。

The length of axons' myelinated segments is important to the success of saltatory conduction. They should be as long as possible to maximize the speed of conduction, but not so long that the arriving signal is too weak to provoke an action potential at the next node of Ranvier. In nature, myelinated segments are generally long enough for the passively propagated signal to travel for at least two nodes while retaining enough amplitude to fire an action potential at the second or third node. Thus, the [[safety factor]] of saltatory conduction is high, allowing transmission to bypass nodes in case of injury. However, action potentials may end prematurely in certain places where the safety factor is low, even in unmyelinated neurons; a common example is the branch point of an axon, where it divides into two axons.{{sfn|Bullock|Orkand|Grinnell|1977|p=163}}

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

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

Some diseases degrade myelin and impair saltatory conduction, reducing the conduction velocity of action potentials.<ref group="lower-alpha" name=":5">{{cite journal | vauthors = Miller RH, Mi S | title = Dissecting demyelination | journal = Nature Neuroscience | volume = 10 | issue = 11 | pages = 1351–4 | date = November 2007 | pmid = 17965654 | doi = 10.1038/nn1995 | s2cid = 12441377 }}</ref> The most well-known of these is [[multiple sclerosis]], in which the breakdown of myelin impairs coordinated movement.<ref name=":13">Waxman, SG in {{harvnb|Waxman|2007|loc=''Multiple Sclerosis as a Neurodegenerative Disease'', pp. 333–346.}}</ref>

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有些疾病会降低髓磷脂，损害跳跃式传导，降低动作电位的传导速度.<ref name=":5" group="lower-alpha" /> ~~。其中最著名的是多发性硬化症，髓磷脂的分解妨碍了协调运动t~~.<ref name=":13" />

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有些疾病会降低髓磷脂，损害跳跃式传导，降低动作电位的传导速度.<ref name=":5" group="lower-alpha" /> 。其中最著名的是多发性硬化症，髓磷脂的破裂妨碍了协调运动t.<ref name=":13" />

===电缆学说 Cable theory===

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The flow of currents within an axon can be described quantitatively by [[cable theory]]<ref name="rall_1989">[[Wilfrid Rall|Rall, W]] in {{harvnb|Koch|Segev|1989|loc=''Cable Theory for Dendritic Neurons'', pp. 9–62.}}</ref> and its elaborations, such as the compartmental model.<ref name="segev_1989">{{cite book | vauthors = Segev I, Fleshman JW, Burke RE | chapter = Compartmental Models of Complex Neurons | title = Methods in Neuronal Modeling: From Synapses to Networks. | veditors = Koch C, Segev I | editor1-link = Christof Koch | date = 1989 | pages = 63–96 | publisher = The MIT Press | location = Cambridge, Massachusetts | isbn = 978-0-262-11133-1 | lccn = 88008279 | oclc = 18384545 }}</ref> Cable theory was developed in 1855 by [[William Thomson, 1st Baron Kelvin|Lord Kelvin]] to model the transatlantic telegraph cable<ref name="kelvin_1855" group=lower-alpha>{{cite journal | vauthors = Kelvin WT | year = 1855 | title = On the theory of the electric telegraph | journal = Proceedings of the Royal Society | volume = 7 | pages = 382–99 | doi = 10.1098/rspl.1854.0093| s2cid = 178547827 | author-link = William Thomson, 1st Baron Kelvin }}</ref> and was shown to be relevant to neurons by [[Alan Lloyd Hodgkin|Hodgkin]] and [[W. A. H. Rushton|Rushton]] in 1946.<ref name="hodgkin_1946" group=lower-alpha>{{cite journal | vauthors = Hodgkin AL, Rushton WA | title = The electrical constants of a crustacean nerve fibre | journal = Proceedings of the Royal Society of Medicine | volume = 134 | issue = 873 | pages = 444–79 | date = December 1946 | pmid = 20281590 | doi = 10.1098/rspb.1946.0024 | author-link1 = Alan Lloyd Hodgkin | bibcode = 1946RSPSB.133..444H | doi-access = free }}</ref> In simple cable theory, the neuron is treated as an electrically passive, perfectly cylindrical transmission cable, which can be described by a [[partial differential equation]]<ref name="rall_1989" />

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轴突内电流的流动可以用电缆理论（cable theory）<ref name="rall_1989" /> ~~及其细致化，如来定量描述。~~.<ref name="segev_1989" /> ~~凯布尔理论是在1855年由开尔文勋爵发展起来用来模拟跨大西洋电报电缆的ble~~<ref name="kelvin_1855" group="lower-alpha" /> ~~a，并在1946年被~~ Hodgkin 和 Rushton ~~证明与神经元有关6.~~<ref name="hodgkin_1946" group="lower-alpha" /> ~~。在简单的电缆理论中，神经元被看作是一根完美的电无源圆柱形传输电缆，可以用偏微分方程来描述~~<ref name="rall_1989" />

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轴突内电流的流动可以用电缆理论（cable theory）<ref name="rall_1989" /> 及其细致化，如房室模型来定量描述。.<ref name="segev_1989" /> 电缆理论是在1855年由开尔文勋爵发展起来用来跨大西洋电报电缆的建模 <ref name="kelvin_1855" group="lower-alpha" />，并在1946年被 Hodgkin 和 Rushton 证明与神经元很有价值。<ref name="hodgkin_1946" group="lower-alpha" /> 在简单的电缆理论中，神经元被看作是一根完美的电无源圆柱形传输电缆，可以用偏微分方程来描述<ref name="rall_1989" />

:<math>

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

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where ''V''（''x'', ''t''） is the voltage across the membrane at a time ''t'' and a position ''x'' along the length of the neuron, and where λ and τ are the characteristic length and time scales on which those voltages decay in response to a stimulus. Referring to the circuit diagram on the right, these scales can be determined from the resistances and capacitances per unit length.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|pp=52–53}}

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

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其中 v （x，t）是跨膜电压在时间 t 和沿神经元长度的位置 x，其中 λ 和 τ 是特征性的长度和时间尺度，对刺激的反应电位的衰减。参考右边的电路图，这些比例可以通过单位长度的电阻和电容来确定。

:<math>

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

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

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

==Termination 终止==

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In general, action potentials that reach the synaptic knobs cause a [[neurotransmitter]] to be released into the synaptic cleft.<ref group="lower-alpha" name=":6">{{cite book | vauthors = Süudhof TC | title = Pharmacology of Neurotransmitter Release | chapter = Neurotransmitter release | volume = 184 | issue = 184 | pages = 1–21 | year = 2008 | pmid = 18064409 | doi = 10.1007/978-3-540-74805-2_1 | isbn = 978-3-540-74804-5 | series = Handbook of Experimental Pharmacology }}</ref> Neurotransmitters are small molecules that may open ion channels in the postsynaptic cell; most axons have the same neurotransmitter at all of their termini. The arrival of the action potential opens voltage-sensitive calcium channels in the presynaptic membrane; the influx of calcium causes [[synaptic vesicle|vesicles]] filled with neurotransmitter to migrate to the cell's surface and [[exocytosis|release their contents]] into the [[synaptic cleft]].<ref group="lower-alpha" name=":7">{{cite journal | vauthors = Rusakov DA | title = Ca2+-dependent mechanisms of presynaptic control at central synapses | journal = The Neuroscientist | volume = 12 | issue = 4 | pages = 317–26 | date = August 2006 | pmid = 16840708 | pmc = 2684670 | doi = 10.1177/1073858405284672 }}</ref> This complex process is inhibited by the [[neurotoxin]]s [[tetanospasmin]] and [[botulinum toxin]], which are responsible for [[tetanus]] and [[botulism]], respectively.<ref group="lower-alpha" name=":8">{{cite journal | vauthors = Humeau Y, Doussau F, Grant NJ, Poulain B | title = How botulinum and tetanus neurotoxins block neurotransmitter release | journal = Biochimie | volume = 82 | issue = 5 | pages = 427–46 | date = May 2000 | pmid = 10865130 | doi = 10.1016/S0300-9084(00)00216-9 }}</ref>

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~~一般来说，到达突触节点的动作电位会使神经递质释放到突触间隙。~~<ref name=":6" group="lower-alpha" /> 神经递质是可以打开突触后细胞离子通道的小分子; 大多数轴突在所有末端都有相同的神经递质。动作电位的到来打开了突触前膜上的电压敏感性钙通道，钙的内流导致充满神经递质的小泡迁移到细胞表面，并将其内容物释放到突触间隙。<ref name=":7" group="lower-alpha" /> 破伤风和肉毒杆菌毒素分别引起神经毒素破伤风和肉毒杆菌毒素抑制这一复杂的过程。<ref name=":8" group="lower-alpha" />

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一般来说，到达突触扣结（synaptic knobs）突触节点的动作电位会使神经递质释放到突触间隙。<ref name=":6" group="lower-alpha" /> 神经递质是可以打开突触后细胞离子通道的小分子；大多数轴突在所有末端都有相同的神经递质。动作电位的到来打开了突触前膜上的电压敏感性钙通道，钙的内流导致充满神经递质的囊泡（vesicle）迁移到细胞表面，并将其内容物释放到突触间隙。<ref name=":7" group="lower-alpha" /> 破伤风和肉毒杆菌毒素分别引起神经毒素破伤风和肉毒杆菌毒素抑制这一复杂的过程。<ref name=":8" group="lower-alpha" />

[[Image:Gap cell junction-en.svg|thumb|right|[[Electrical synapse]]s between excitable cells allow ions to pass directly from one cell to another, and are much faster than [[chemical synapse]]s.

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Some synapses dispense with the "middleman" of the neurotransmitter, and connect the presynaptic and postsynaptic cells together.<ref group="lower-alpha" name=":9">{{cite journal | vauthors = Zoidl G, Dermietzel R | title = On the search for the electrical synapse: a glimpse at the future | journal = Cell and Tissue Research | volume = 310 | issue = 2 | pages = 137–42 | date = November 2002 | pmid = 12397368 | doi = 10.1007/s00441-002-0632-x | s2cid = 22414506 }}</ref> When an action potential reaches such a synapse, the ionic currents flowing into the presynaptic cell can cross the barrier of the two cell membranes and enter the postsynaptic cell through pores known as [[connexon]]s.<ref group="lower-alpha" name=":10">{{cite journal | vauthors = Brink PR, Cronin K, Ramanan SV | title = Gap junctions in excitable cells | journal = Journal of Bioenergetics and Biomembranes | volume = 28 | issue = 4 | pages = 351–8 | date = August 1996 | pmid = 8844332 | doi = 10.1007/BF02110111 | s2cid = 46371790 }}</ref> Thus, the ionic currents of the presynaptic action potential can directly stimulate the postsynaptic cell. Electrical synapses allow for faster transmission because they do not require the slow diffusion of [[neurotransmitter]]s across the synaptic cleft. Hence, electrical synapses are used whenever fast response and coordination of timing are crucial, as in [[escape reflex]]es, the [[retina]] of [[vertebrate]]s, and the [[heart]].

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~~有些突触免除了神经递质的“中间人”，将突触前细胞和突触后细胞连接在一起。~~<ref name=":9" group="lower-alpha" /> 当一个动作电位达到这样的突触时，流入突触前细胞的离子电流可以穿过两个细胞膜的屏障，通过称为连接子的孔进入突触后细胞。<ref name=":10" group="lower-alpha" /> 因此，突触前动作电位的离子电流可以直接刺激突触后细胞。电突触允许更快的传递，因为它们不需要神经递质在突触间隙中的缓慢扩散。因此，只要快速反应和协调时间是至关重要的，就会使用电突触，例如在逃跑反射、脊椎动物的视网膜和心脏中。

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有些突触免除了神经递质的“中间人”，而将突触前细胞和突触后细胞连接在一起。<ref name=":9" group="lower-alpha" /> 当一个动作电位达到这样的突触时，流入突触前细胞的离子电流可以穿过两个细胞膜的屏障，通过称为连接子的孔进入突触后细胞。<ref name=":10" group="lower-alpha" /> 因此，突触前动作电位的离子电流可以直接刺激突触后细胞。电突触允许更快的传递，因为它们不需要神经递质在突触间隙中的缓慢扩散。因此，只要快速反应和协调时间是至关重要的，就会使用电突触，例如在逃跑反射、脊椎动物的视网膜和心脏中。

===神经肌肉接头Neuromuscular junctions===

A special case of a chemical synapse is the [[neuromuscular junction]], in which the [[axon]] of a [[motor neuron]] terminates on a [[muscle fiber]].<ref group="lower-alpha" name=":11">{{cite journal | vauthors = Hirsch NP | title = Neuromuscular junction in health and disease | journal = British Journal of Anaesthesia | volume = 99 | issue = 1 | pages = 132–8 | date = July 2007 | pmid = 17573397 | doi = 10.1093/bja/aem144 | df = dmy-all | doi-access = free }}</ref> In such cases, the released neurotransmitter is [[acetylcholine]], which binds to the acetylcholine receptor, an integral membrane protein in the membrane （the ''[[sarcolemma]]''） of the muscle fiber.<ref group="lower-alpha" name=":12">{{cite journal | vauthors = Hughes BW, Kusner LL, Kaminski HJ | title = Molecular architecture of the neuromuscular junction | journal = Muscle & Nerve | volume = 33 | issue = 4 | pages = 445–61 | date = April 2006 | pmid = 16228970 | doi = 10.1002/mus.20440 | s2cid = 1888352 }}</ref> However, the acetylcholine does not remain bound; rather, it dissociates and is [[hydrolysis|hydrolyzed]] by the enzyme, [[acetylcholinesterase]], located in the synapse. This enzyme quickly reduces the stimulus to the muscle, which allows the degree and timing of muscular contraction to be regulated delicately. Some poisons inactivate acetylcholinesterase to prevent this control, such as the [[nerve agent]]s [[sarin]] and [[tabun (nerve agent)|tabun]],<ref name=Newmark group=lower-alpha>{{cite journal | vauthors = Newmark J | title = Nerve agents | journal = The Neurologist | volume = 13 | issue = 1 | pages = 20–32 | date = January 2007 | pmid = 17215724 | doi = 10.1097/01.nrl.0000252923.04894.53 | s2cid = 211234081 }}</ref> and the insecticides [[diazinon]] and [[malathion]].<ref group="lower-alpha" name=":13">{{cite journal | vauthors = Costa LG | title = Current issues in organophosphate toxicology | journal = Clinica Chimica Acta; International Journal of Clinical Chemistry | volume = 366 | issue = 1–2 | pages = 1–13 | date = April 2006 | pmid = 16337171 | doi = 10.1016/j.cca.2005.10.008 }}</ref>

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突触间隙的一个特例是神经肌肉接点（neuromuscular junction），运动神经元的轴突终止于肌纤维上。<ref name=":11" group="lower-alpha" /> ~~在这种情况下，释放出来的神经递质是乙酰胆碱，它结合在肌肉纤维膜（肌膜）上的乙酰胆碱受体膜内在蛋白。~~<ref name=":12" group="lower-alpha" /> 然而，乙酰胆碱并不保持结合状态，而是分解并被位于突触中的乙酰胆碱酯酶水解。这种酶能迅速减少对肌肉的刺激，从而使肌肉收缩的程度和时间得到精细的调节。一些毒药使乙酰胆碱酯酶失活，以防止这种控制，如神经毒剂沙林和塔崩，<ref name="Newmark" group="lower-alpha" /> 以及杀虫剂二嗪农和马拉硫磷。<ref name=":13" group="lower-alpha" />

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突触间隙的一个特例是神经肌肉接点（neuromuscular junction），运动神经元的轴突终止于肌纤维上。<ref name=":11" group="lower-alpha" /> 在这种情况下，释放出来的神经递质是乙酰胆碱，它结合在肌肉纤维膜（肌膜）上的内在膜蛋白乙酰胆碱受体。<ref name=":12" group="lower-alpha" /> 然而，乙酰胆碱并不保持结合状态，而是解离并被位于突触中的乙酰胆碱酯酶水解。这种酶能迅速减少对肌肉的刺激，从而使肌肉收缩的程度和时间得到精细的调节。一些毒药使乙酰胆碱酯酶失活，以阻断这种控制，如神经毒剂沙林和塔崩，<ref name="Newmark" group="lower-alpha" /> 以及杀虫剂二嗪农和马拉硫磷。<ref name=":13" group="lower-alpha" />

==Other cell types 其他细胞类型==

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[[Image:Ventricular myocyte action potential.svg|thumb|220px|[[文件:Ventricular myocyte action potential.svg.png|缩略图]]Phases of a cardiac action potential. The sharp rise in voltage （"0"） corresponds to the influx of sodium ions, whereas the two decays （"1" and "3", respectively） correspond to the sodium-channel inactivation and the repolarizing eflux of potassium ions. The characteristic plateau （"2"） results from the opening of voltage-sensitive [[calcium]] channels.

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

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

The cardiac action potential differs from the neuronal action potential by having an extended plateau, in which the membrane is held at a high voltage for a few hundred milliseconds prior to being repolarized by the potassium current as usual.<ref name=Kleber group=lower-alpha /> This plateau is due to the action of slower [[calcium]] channels opening and holding the membrane voltage near their equilibrium potential even after the sodium channels have inactivated.

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

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心肌动作电位与神经元动作电位的不同之处在于，心肌动作电位有一个延长的平台期，在这个平台期间，膜在被钾电流复极化之前以高电位保持几百毫秒。<ref name="Kleber" group="lower-alpha" /> 这个平台是由于慢速钙通道打开的作用，即使在钠通道失去活性之后，仍然保持膜电位接近其平衡电位。

The cardiac action potential plays an important role in coordinating the contraction of the heart.<ref name=Kleber group=lower-alpha>{{cite journal | vauthors = Kléber AG, Rudy Y | title = Basic mechanisms of cardiac impulse propagation and associated arrhythmias | journal = Physiological Reviews | volume = 84 | issue = 2 | pages = 431–88 | date = April 2004 | pmid = 15044680 | doi = 10.1152/physrev.00025.2003 | s2cid = 21823003 }}</ref> The cardiac cells of the [[sinoatrial node]] provide the [[pacemaker potential]] that synchronizes the heart. The action potentials of those cells propagate to and through the [[atrioventricular node]] （AV node）, which is normally the only conduction pathway between the [[atrium (heart)|atria]] and the [[ventricle (heart)|ventricles]]. Action potentials from the AV node travel through the [[bundle of His]] and thence to the [[Purkinje fiber]]s.<ref group="note" name=":0">Note that these [[Purkinje fiber]]s are muscle fibers and not related to the [[Purkinje cell]]s, which are [[neuron]]s found in the [[cerebellum]].</ref> Conversely, anomalies in the cardiac action potential—whether due to a congenital mutation or injury—can lead to human pathologies, especially [[Heart arrhythmia|arrhythmia]]s.<ref name=Kleber group=lower-alpha /> Several anti-arrhythmia drugs act on the cardiac action potential, such as [[quinidine]], [[lidocaine]], [[beta blocker]]s, and [[verapamil]].<ref group="lower-alpha" name=":14">{{cite journal | vauthors = Tamargo J, Caballero R, Delpón E | title = Pharmacological approaches in the treatment of atrial fibrillation | journal = Current Medicinal Chemistry | volume = 11 | issue = 1 | pages = 13–28 | date = January 2004 | pmid = 14754423 | doi = 10.2174/0929867043456241 }}</ref>

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~~心脏动作电位在协调心脏收缩中起着重要作用。窦房结的心脏细胞提供了同步心脏的起搏器电位。~~<ref name="Kleber" group="lower-alpha" /> 这些细胞的动作电位传导到并通过房室结，这通常是心房和心室之间唯一的传导通路。房室结的动作电位通过 His ~~束传递到浦肯野纤维。请注意，这些浦肯野纤维是肌纤维，与浦肯野细胞无关，浦肯野细胞是小脑中的神经元。~~<ref name=":0" group="note" /> ~~相反，心脏动作电位的异常ーー无论是由于先天性突变还是损伤ーー都可能导致人类疾病，尤其是心律失常。~~<ref name="Kleber" group="lower-alpha" /> ~~几种抗心律失常药物作用于心脏动作电位，如奎尼丁、利多卡因、~~ β 受体阻滞剂和维拉帕米。<ref name=":14" group="lower-alpha" />

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心肌动作电位在协调心脏收缩中起着重要作用。窦房结的心脏细胞提供了同步心脏的起搏器电位。<ref name="Kleber" group="lower-alpha" /> 这些细胞的动作电位传导到并通过房室结，这通常是心房和心室之间唯一的传导通路。房室结的动作电位通过 His 束传递到浦肯野纤维。请注意，这些浦肯野纤维是肌纤维，与小脑中的神经元浦肯野细胞无关。<ref name=":0" group="note" /> 相反，心肌动作电位的异常ーー无论是由于先天性突变还是损伤ーー都可能导致人类疾病，尤其是心律失常。<ref name="Kleber" group="lower-alpha" /> 几种抗心律失常药物作用于心肌动作电位，如奎尼丁、利多卡因、 β 受体阻滞剂和维拉帕米。<ref name=":14" group="lower-alpha" />

===肌肉动作电位 Muscular action potentials===

The action potential in a normal skeletal muscle cell is similar to the action potential in neurons.{{sfn|Ganong|1991|pp=59–60}} Action potentials result from the depolarization of the cell membrane （the [[sarcolemma]]）, which opens voltage-sensitive sodium channels; these become inactivated and the membrane is repolarized through the outward current of potassium ions. The resting potential prior to the action potential is typically −90mV, somewhat more negative than typical neurons. The muscle action potential lasts roughly 2–4 ms, the absolute refractory period is roughly 1–3 ms, and the conduction velocity along the muscle is roughly 5 m/s. The action potential releases [[calcium]] ions that free up the [[tropomyosin]] and allow the muscle to contract. Muscle action potentials are provoked by the arrival of a pre-synaptic neuronal action potential at the [[neuromuscular junction]], which is a common target for [[neurotoxin]]s.<ref name=Newmark group=lower-alpha />

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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（性）约为1~~-3ms，肌肉传导速度约为5 m/s。动作电位释放钙离子，释放原肌球蛋白，使肌肉收缩。肌肉动作电位是由突触前神经元动作电位在神经肌肉接点的到达引起的，这是神经毒素的一个共同目标。<ref name="Newmark" group="lower-alpha" />

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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" />

===植物动作电位Plant action potentials===

[[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" /> ~~也是电性兴奋的。与动物动作电位的根本区别在于，植物细胞的去极化不是通过吸收正钠离子来完成的，而是通过释放负氯离子来完成的。~~<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" />

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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However, plenty of research has been done on action potentials and how they affect movement and clockwork within the Venus flytrap. To start, the resting membrane potential of the Venus flytrap （-120mV） is lower than animal cells （usually -90mV to -40mV）.<ref name=":2" /><ref name=":17">Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Neuroscience. 2nd edition. Sunderland (MA): Sinauer Associates; 2001. Electrical Potentials Across Nerve Cell Membranes.Available from: <nowiki>https://www.ncbi.nlm.nih.gov/books/NBK11069/</nowiki></ref> The lower resting potential makes it easier to activate an action potential. Thus, when an insect lands on the trap of the plant, it triggers a hair-like mechanoreceptor.<ref name=":2" /> This receptor then activates an action potential which lasts around 1.5 ms.<ref name=":18">{{cite journal | vauthors = Volkov AG, Adesina T, Jovanov E | title = Closing of venus flytrap by electrical stimulation of motor cells | journal = Plant Signaling & Behavior | volume = 2 | issue = 3 | pages = 139–45 | date = May 2007 | pmid = 19516982 | pmc = 2634039 | doi = 10.4161/psb.2.3.4217 }}</ref> Ultimately, this causes an increase of positive Calcium ions into the cell, slightly depolarizing it.

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然而，已经有很多关于动作电位以及它们如何影响捕蝇草内的运动和钟表的研究。首先，捕蝇草的静息膜电位（- 120mV）低于动物细胞（通常为-90mv 至-40mv）。<ref name=":2" /><ref name=":17" /> 神经细胞膜上的电位。的静息电位可以更容易地激活动作电位。因此，当一只昆虫落在植物的陷阱上时，它就会触发一个毛发样的机械感受器。.<ref name=":2" /> 低这个受体激活一个持续约1.5毫秒的动作电位。<ref name=":18" /> 最终，这会导致钙离子进入细胞，使细胞稍微去极化。 [https://www.ncbi.nlm.nih.gov/books/nbk11069/的静息电位可以更容易地激活动作电位。因此，当一只昆虫落在植物的陷阱上时，它就会触发一个毛发样的机械感受器。这个受体激活一个持续约1.5毫秒的动作电位。最终，这会导致钙离子进入细胞，使细胞稍微去极化。 https://www.ncbi.nlm.nih.gov/books/nbk11069/]

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然而，已经有很多关于动作电位以及它们如何影响捕蝇草内的运动和钟表的研究。首先，捕蝇草的静息膜电位（- 120mV）低于动物细胞（通常为-90mv 至-40mv）。<ref name=":2" /><ref name=":17" /> 神经细胞膜上的电位。的静息电位可以更容易地激活动作电位。因此，当一只昆虫落在植物的陷阱上时，它就会触发一个毛发样的机械感受器。.<ref name=":2" /> 低这个受体激活一个持续约1.5毫秒的动作电位。<ref name=":18" /> 最终，这会导致钙离子进入细胞，使细胞稍微去极化。

However, the flytrap doesn't close after one trigger. Instead, it requires the activation of 2 or more hairs.<ref name=":1" /><ref name=":2" /> If only one hair is triggered, it throws the activation as a false positive. Further, the second hair must be activated within a certain time interval （0.75 s - 40 s） for it to register with the first activation.<ref name=":2" /> Thus, a buildup of calcium starts and slowly falls from the first trigger. When the second action potential is fired within the time interval, it reaches the Calcium threshold to depolarize the cell, closing the trap on the prey within a fraction of a second.<ref name=":2" />

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Given its conservation throughout evolution, the action potential seems to confer evolutionary advantages. One function of action potentials is rapid, long-range signaling within the organism; the conduction velocity can exceed 110 m/s, which is one-third the [[speed of sound]]. For comparison, a hormone molecule carried in the bloodstream moves at roughly 8 m/s in large arteries. Part of this function is the tight coordination of mechanical events, such as the contraction of the heart. A second function is the computation associated with its generation. Being an all-or-none signal that does not decay with transmission distance, the action potential has similar advantages to [[digital electronics]]. The integration of various dendritic signals at the axon hillock and its thresholding to form a complex train of action potentials is another form of computation, one that has been exploited biologically to form [[central pattern generator]]s and mimicked in [[artificial neural network]]s.

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鉴于动作电位在整个进化过程中的保守性，它似乎赋予了进化优势。动作电位的一个功能是在生物体内快速的远程信号传导，传导速度可以超过110米/秒，这是声速的三分之一。相比之下，血液中携带的荷尔蒙分子在大动脉中的运动速度大约为每秒8米。这个功能的一部分是机械事件的紧密协调，例如心脏的收缩。第二个函数是与其生成相关的计算。动作电位作为一种全或无信号，不随传输距离衰减，与数字电子技术具有相似的优点。轴突小丘上各种树突信号的整合及其阈值化形成一系列复杂的动作电位是另一种形式的计算方法，这种方法已被生物学方法用来形成中心模式发生器，并在人工神经网络中进行模拟。

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鉴于动作电位在整个进化过程中的保守性，它似乎赋予了进化优势。动作电位的一个功能是在生物体内快速的远程信号传导，传导速度可以超过110米/秒，这是声速的三分之一。相比之下，血液中携带的荷尔蒙分子在大动脉中的运动速度大约为每秒8米。这个功能的一部分是机械事件的紧密协调，例如心脏的收缩。第二个功能是与其生成相关的计算。动作电位作为一种全或无信号，不随传输距离衰减，与数字电子技术具有相似的优点。轴突小丘上各种树突信号的整合及其阈值化形成一系列复杂的动作电位是另一种形式的计算方法，这种方法已被生物学方法用来形成中心模式发生器，并在人工神经网络中进行模拟。

The common prokaryotic/eukaryotic ancestor, which lived perhaps four billion years ago, is believed to have had voltage-gated channels. This functionality was likely, at some later point, cross-purposed to provide a communication mechanism. Even modern single-celled bacteria can utilize action potentials to communicate with other bacteria in the same biofilm.<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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==实验方法Experimental methods==

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

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[[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]]

The study of action potentials has required the development of new experimental methods. The initial work, prior to 1955, was carried out primarily by [[Alan Lloyd Hodgkin]] and [[Andrew Fielding Huxley]], who were, along [[John Carew Eccles]], awarded the 1963 [[Nobel Prize in Physiology or Medicine]] for their contribution to the description of the ionic basis of nerve conduction. It focused on three goals: isolating signals from single neurons or axons, developing fast, sensitive electronics, and shrinking [[electrode]]s enough that the voltage inside a single cell could be recorded.

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动作电位的研究需要开发新的实验方法。在 1955 年之前，最初的工作主要是由艾伦·劳埃德·霍奇金和 Andrew Fielding Huxley 完成的，他们因为在描述神经传导的离子基础方面做出的贡献，和约翰·卡鲁·埃克尔斯一起被授予 1963 年诺贝尔生理学或医学奖。它着重于三个目标: 从单个神经元或轴突中分离出信号，发展快速、灵敏的电子设备，以及缩小电极，使单个细胞内的电压能够被记录下来。

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动作电位的研究需要开发新的实验方法。在 1955 年之前，最初的工作主要是由艾伦·劳埃德·霍奇金和 Andrew Fielding Huxley 完成的，他们因为在描述神经传导的离子基础方面做出的贡献，和约翰·卡鲁·埃克尔斯一起被授予 1963 年诺贝尔生理学或医学奖。它着重于三个目标：从单个神经元或轴突中分离出信号，发展快速、灵敏的电子设备，以及缩小电极，使单个细胞内的电压能够被记录下来。

The first problem was solved by studying the [[Squid giant axon|giant axons]] found in the neurons of the [[squid]] （''[[Loligo forbesii]]'' and ''[[Doryteuthis pealeii]]'', at the time classified as ''Loligo pealeii''）.<ref name="keynes_1989" group="lower-alpha">{{cite journal | vauthors = Keynes RD | title = The role of giant axons in studies of the nerve impulse | journal = BioEssays | volume = 10 | issue = 2–3 | pages = 90–3 | year = 1989 | pmid = 2541698 | doi = 10.1002/bies.950100213 }}</ref> These axons are so large in diameter （roughly 1 mm, or 100-fold larger than a typical neuron） that they can be seen with the naked eye, making them easy to extract and manipulate.<ref name="hodgkin_1952" group="lower-alpha" /><ref name="Meunier" group="lower-alpha">{{cite journal | vauthors = Meunier C, Segev I | title = Playing the devil's advocate: is the Hodgkin-Huxley model useful? | journal = Trends in Neurosciences | volume = 25 | issue = 11 | pages = 558–63 | date = November 2002 | pmid = 12392930 | doi = 10.1016/S0166-2236(02)02278-6 | s2cid = 1355280 }}</ref> However, they are not representative of all excitable cells, and numerous other systems with action potentials have been studied.

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第一个问题通过研究乌贼神经元中发现的巨大轴突（Loligo forbesii 和 Doryteuthis pealeii，当时被归类为 Loligo pealeii）得到了解决。<ref name="keynes_1989" group="lower-alpha" /> 这些轴突直径很大（大约1毫米，比一个典型的神经元大100倍），可以用肉眼看到，因此很容易提取和操作。<ref name="hodgkin_1952" group="lower-alpha" /><ref name="Meunier" group="lower-alpha" /> ~~然而，它们并不代表所有可兴奋细胞，许多其他具有动作电位的系统已被研究。~~

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第一个问题通过研究乌贼神经元中发现的巨大轴突（Loligo forbesii 和 Doryteuthis pealeii，当时被归类为 Loligo pealeii）得到了解决。<ref name="keynes_1989" group="lower-alpha" /> 这些轴突直径很大（大约1毫米，比一个典型的神经元大100倍），可以用肉眼看到，因此很容易提取和操作。<ref name="hodgkin_1952" group="lower-alpha" /><ref name="Meunier" group="lower-alpha" /> 然而，它们并不代表所有可兴奋细胞，许多其他有动作电位的系统已被研究。

The second problem was addressed with the crucial development of the [[voltage clamp]],<ref name="cole_1949" group="lower-alpha">{{cite journal | vauthors = Cole KS | year = 1949 | title = Dynamic electrical characteristics of the squid axon membrane | journal = Arch. Sci. Physiol. | volume = 3 | pages = 253–8| author-link = Kenneth Stewart Cole }}</ref> which permitted experimenters to study the ionic currents underlying an action potential in isolation, and eliminated a key source of [[electronic noise]], the current ''IC'' associated with the [[capacitance]] ''C'' of the membrane.{{sfn|Junge|1981|pp=63–82}} Since the current equals ''C'' times the rate of change of the transmembrane voltage ''Vm'', the solution was to design a circuit that kept ''Vm'' fixed （zero rate of change） regardless of the currents flowing across the membrane. Thus, the current required to keep ''Vm'' at a fixed value is a direct reflection of the current flowing through the membrane. Other electronic advances included the use of [[Faraday cage]]s and electronics with high [[input impedance]], so that the measurement itself did not affect the voltage being measured.{{sfn|Kettenmann|Grantyn|1992}}

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第二个问题是关于电压钳,<ref name="cole_1949" group="lower-alpha" /> ~~的关键发展，它允许实验者在隔离的情况下研究作用于动作电位的离子电流，并消除了电子噪声的一个关键来源~~---- 与膜电容 c 相关的电流 IC。由于电流等于 c 乘以跨膜电压 Vm 的变化率，所以解决方案是设计一个电路，使 Vm 保持固定（零变化率），而不管跨膜电流的变化。因此，使 Vm 保持在一个固定值所需的电流是流过薄膜的电流的直接反射。其他电子方面的进步包括使用法拉第笼和具有高输入阻抗的电子器件，这样测量本身就不会影响被测量的电压。

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第二个问题是关于电压钳,<ref name="cole_1949" group="lower-alpha" /> 的关键发展，它允许实验者在分离的情况下研究作用于动作电位的离子电流，并消除了电子噪声的一个关键来源---- 与膜电容 c''C'' 相关的电流 ''IC'' IC。由于电流等于''C'' c 乘以跨膜电压 ''Vm'' 的变化率，所以解决方案是设计一个电路，使 ''Vm'' 保持固定（零变化率），而不管跨膜电流的变化。因此，使 ''Vm'' Vm 保持在一个固定值所需的电流是流过薄膜的电流的直接反射。其他电子方面的进步包括使用法拉第笼和具有高输入阻抗的电子器件，这样测量本身就不会影响被测量的电压。

The third problem, that of obtaining electrodes small enough to record voltages within a single axon without perturbing it, was solved in 1949 with the invention of the glass micropipette electrode,<ref name="ling_1949" group="lower-alpha">{{cite journal | vauthors = Ling G, Gerard RW | title = The normal membrane potential of frog sartorius fibers | journal = Journal of Cellular and Comparative Physiology | volume = 34 | issue = 3 | pages = 383–96 | date = December 1949 | pmid = 15410483 | doi = 10.1002/jcp.1030340304 }}</ref> which was quickly adopted by other researchers.<ref name="nastuk_1950" group="lower-alpha">{{cite journal | vauthors = Nastuk WL, Hodgkin A | year = 1950 | title = The electrical activity of single muscle fibers | journal = Journal of Cellular and Comparative Physiology | volume = 35 | pages = 39–73 | doi = 10.1002/jcp.1030350105 }}</ref><ref name="brock_1952" group="lower-alpha">{{cite journal | vauthors = Brock LG, Coombs JS, Eccles JC | title = The recording of potentials from motoneurones with an intracellular electrode | journal = The Journal of Physiology | volume = 117 | issue = 4 | pages = 431–60 | date = August 1952 | pmid = 12991232 | pmc = 1392415 | doi = 10.1113/jphysiol.1952.sp004759 }}</ref> Refinements of this method are able to produce electrode tips that are as fine as 100 [[Ångström|Å]] （10 [[nanometre|nm]]）, which also confers high input impedance.<ref name=":20">Snell, FM in {{harvnb|Lavallée|Schanne|Hébert|1969|loc=''Some Electrical Properties of Fine-Tipped Pipette Microelectrodes''.}}</ref> Action potentials may also be recorded with small metal electrodes placed just next to a neuron, with [[neurochip]]s containing [[EOSFET]]s, or optically with dyes that are [[Calcium imaging|sensitive to Ca2+]] or to voltage.<ref name="dyes" group="lower-alpha">{{cite journal | vauthors = Ross WN, Salzberg BM, Cohen LB, Davila HV | title = A large change in dye absorption during the action potential | journal = Biophysical Journal | volume = 14 | issue = 12 | pages = 983–6 | date = December 1974 | pmid = 4429774 | pmc = 1334592 | doi = 10.1016/S0006-3495(74)85963-1 | bibcode = 1974BpJ....14..983R }} * {{cite journal | vauthors = Grynkiewicz G, Poenie M, Tsien RY | title = A new generation of Ca2+ indicators with greatly improved fluorescence properties | journal = The Journal of Biological Chemistry | volume = 260 | issue = 6 | pages = 3440–50 | date = March 1985 | doi = 10.1016/S0021-9258(19)83641-4 | pmid = 3838314 | doi-access = free }}</ref>

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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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一些天然和人工的神经毒素被设计用来阻断动作电位。来自河豚的河豚毒素和来自沟鞭藻属的石房蛤毒素通过抑制电压敏感性钠通道来阻断动作电位；同样地，黑曼巴蛇的树眼镜蛇毒素也会抑制电压敏感性钾离子通道。这种离子通道的抑制剂有一个重要的研究目的，它可以让科学家随意关闭特定的通道，从而分离出其他通道的贡献；它们也可以用亲和色谱法来净化离子通道或测定它们的浓度。然而，这些抑制剂也能产生有效的神经毒素，并被认为是化学武器。针对昆虫离子通道的神经毒素一直是有效的杀虫剂，其中一个例子是合成氯菊酯，它延长了与动作电位有关的钠通道的激活。昆虫的离子通道与人类的离子通道完全不同，因此对人类几乎没有副作用。

==History历史==

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

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

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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s<ref name="FRET" group="lower-alpha" /> 和冷冻电子显微研究s.<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" />。

==定量模型Quantitative models==

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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" /> ~~c，computationn~~<ref name="computational_studies" /> ~~Nelson，ME; Rinzel，j in </> * Rinzel，j & ertrout，GB; in electronics.~~<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太平洋小体.~~<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" />。

==Notes==

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