更改

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

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

===发生===

===动作电位的触发===

Before considering the propagation of action potentials along [[axon]]s and their termination at the synaptic knobs, it is helpful to consider the methods by which action potentials can be initiated at the [[axon hillock]]. The basic requirement is that the membrane voltage at the hillock be raised above the threshold for firing. There are several ways in which this depolarization can occur.

Before considering the propagation of action potentials along [[axon]]s and their termination at the synaptic knobs, it is helpful to consider the methods by which action potentials can be initiated at the [[axon hillock]]. The basic requirement is that the membrane voltage at the hillock be raised above the threshold for firing. There are several ways in which this depolarization can occur.

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

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

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]]

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]]

===动力学===

===动作电位的动力学===

Action potentials are most commonly initiated by [[excitatory postsynaptic potential]]s from a presynaptic neuron.{{sfnm|1a1=Bullock|1a2=Orkand|1a3=Grinnell|1y=1977|1pp=177–240|2a1=Schmidt-Nielsen|2y=1997|2pp=490-499|3a1=Stevens|3y=1966|3p=47–68}} Typically, [[neurotransmitter]] molecules are released by the [[synapse|presynaptic]] [[neuron]]. These neurotransmitters then bind to receptors on the postsynaptic cell. This binding opens various types of [[ion channel]]s. This opening has the further effect of changing the local permeability of the [[cell membrane]] and, thus, the membrane potential. If the binding increases the voltage （depolarizes the membrane）, the synapse is excitatory. If, however, the binding decreases the voltage （hyperpolarizes the membrane）, it is inhibitory. Whether the voltage is increased or decreased, the change propagates passively to nearby regions of the membrane （as described by the [[cable equation]] and its refinements）. Typically, the voltage stimulus decays exponentially with the distance from the synapse and with time from the binding of the neurotransmitter. Some fraction of an excitatory voltage may reach the [[axon hillock]] and may （in rare cases） depolarize the membrane enough to provoke a new action potential. More typically, the excitatory potentials from several synapses must [[spatial summation|work together]] at [[temporal summation|nearly the same time]] to provoke a new action potential. Their joint efforts can be thwarted, however, by the counteracting [[inhibitory postsynaptic potential]]s.

Action potentials are most commonly initiated by [[excitatory postsynaptic potential]]s from a presynaptic neuron.{{sfnm|1a1=Bullock|1a2=Orkand|1a3=Grinnell|1y=1977|1pp=177–240|2a1=Schmidt-Nielsen|2y=1997|2pp=490-499|3a1=Stevens|3y=1966|3p=47–68}} Typically, [[neurotransmitter]] molecules are released by the [[synapse|presynaptic]] [[neuron]]. These neurotransmitters then bind to receptors on the postsynaptic cell. This binding opens various types of [[ion channel]]s. This opening has the further effect of changing the local permeability of the [[cell membrane]] and, thus, the membrane potential. If the binding increases the voltage （depolarizes the membrane）, the synapse is excitatory. If, however, the binding decreases the voltage （hyperpolarizes the membrane）, it is inhibitory. Whether the voltage is increased or decreased, the change propagates passively to nearby regions of the membrane （as described by the [[cable equation]] and its refinements）. Typically, the voltage stimulus decays exponentially with the distance from the synapse and with time from the binding of the neurotransmitter. Some fraction of an excitatory voltage may reach the [[axon hillock]] and may （in rare cases） depolarize the membrane enough to provoke a new action potential. More typically, the excitatory potentials from several synapses must [[spatial summation|work together]] at [[temporal summation|nearly the same time]] to provoke a new action potential. Their joint efforts can be thwarted, however, by the counteracting [[inhibitory postsynaptic potential]]s.

Neurotransmission can also occur through [[electrical synapse]]s.{{sfnm|1a1=Bullock|1a2=Orkand|1a3=Grinnell|1y=1977|1pp=178–180|2a1=Schmidt-Nielsen|2y=1997|2pp=490-491}} Due to the direct connection between excitable cells in the form of [[gap junction]]s, an action potential can be transmitted directly from one cell to the next in either direction. The free flow of ions between cells enables rapid non-chemical-mediated transmission. Rectifying channels ensure that action potentials move only in one direction through an electrical synapse.{{Citation needed|date=May 2011}} Electrical synapses are found in all nervous systems, including the human brain, although they are a distinct minority.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2001}}

Neurotransmission can also occur through [[electrical synapse]]s.{{sfnm|1a1=Bullock|1a2=Orkand|1a3=Grinnell|1y=1977|1pp=178–180|2a1=Schmidt-Nielsen|2y=1997|2pp=490-491}} Due to the direct connection between excitable cells in the form of [[gap junction]]s, an action potential can be transmitted directly from one cell to the next in either direction. The free flow of ions between cells enables rapid non-chemical-mediated transmission. Rectifying channels ensure that action potentials move only in one direction through an electrical synapse.{{Citation needed|date=May 2011}} Electrical synapses are found in all nervous systems, including the human brain, although they are a distinct minority.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2001}}

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.

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.

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，受体电位的振幅取决于刺激的强度。在这两种情况下，动作电位的频率都与刺激的强度相关。

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。

===Sensory neurons 感觉神经元===

===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]].

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]].

===Pacemaker potentials 起搏电位===

===Pacemaker potentials 起搏电位===

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

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

在感觉神经元中，动作电位来自外部刺激。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" /> 虽然这种起搏器电位具有自然节律，但它可以通过外部刺激进行调节；例如，药物以及交感神经和副交感神经发出的信号可以改变心率。外部刺激不会引起细胞的反复放电，只是改变了它的放电频率。在某些情况下，频率的调节可能更加复杂，导致动作电位的模式，如爆发。

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。

==Phases==

==Phases==

The course of the action potential can be divided into five parts: the rising phase, the peak phase, the falling phase, the undershoot phase, and the refractory period. During the rising phase the membrane potential depolarizes （becomes more positive）. The point at which [[depolarization]] stops is called the peak phase. At this stage, the membrane potential reaches a maximum. Subsequent to this, there is a falling phase. During this stage the membrane potential becomes more negative, returning towards resting potential. The undershoot, or [[afterhyperpolarization]], phase is the period during which the membrane potential temporarily becomes more negatively charged than when at rest （hyperpolarized）. Finally, the time during which a subsequent action potential is impossible or difficult to fire is called the [[refractory period (physiology)|refractory period]], which may overlap with the other phases.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|p=38}}

The course of the action potential can be divided into five parts: the rising phase, the peak phase, the falling phase, the undershoot phase, and the refractory period. During the rising phase the membrane potential depolarizes （becomes more positive）. The point at which [[depolarization]] stops is called the peak phase. At this stage, the membrane potential reaches a maximum. Subsequent to this, there is a falling phase. During this stage the membrane potential becomes more negative, returning towards resting potential. The undershoot, or [[afterhyperpolarization]], phase is the period during which the membrane potential temporarily becomes more negatively charged than when at rest （hyperpolarized）. Finally, the time during which a subsequent action potential is impossible or difficult to fire is called the [[refractory period (physiology)|refractory period]], which may overlap with the other phases.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|p=38}}

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

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

动作电位的过程是由两个耦合效应决定的。首先，电压敏感离子通道的开启和关闭是为了响应膜电位的变化。这改变了膜对这些离子的渗透性。其次，根据戈德曼方程的研究，这种渗透率的变化改变了平衡电位 Em，从而改变了膜电位.<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，但随后由于较慢的失活而关闭。

动作电位的过程是由两个耦合的效应决定的。首先，膜电位的变化引起电压敏感离子通道的打开和关闭，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。

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

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

艾伦·劳埃德·霍奇金和 Andrew Huxley 在1952年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，戈尔丁通道和铝通道s,<ref name="goldin_2007" /> a，它们并不总是独立开启和关闭的y.<ref name=":0" group="lower-alpha" />。

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" />

===Stimulation and rising phase===

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

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

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

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

<nowiki>= = = 刺激和上升期 = = =</nowiki>

 

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。

For a neuron at rest, there is a high concentration of sodium and chloride ions in the [[extracellular fluid]] compared to the [[intracellular fluid]], while there is a high concentration of potassium ions in the intracellular fluid compared to the extracellular fluid. The difference in concentrations, which causes ions to move [[Second law of thermodynamics|from a high to a low concentration]], and electrostatic effects （attraction of opposite charges） are responsible for the movement of ions in and out of the neuron. The inside of a neuron has a negative charge, relative to the cell exterior, from the movement of K⁺ out of the cell. The neuron membrane is more permeable to K⁺ than to other ions, allowing this ion to selectively move out of the cell, down its concentration gradient. This concentration gradient along with [[potassium leak channel]]s present on the membrane of the neuron causes an [[wikt:Special:Search/efflux|efflux]] of potassium ions making the resting potential close to ''E''_K&nbsp;≈&nbsp;–75&nbsp;mV.{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1p=34|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2p=134|3a1=Schmidt-Nielsen|3y=1997|3pp=478–480}} Since Na⁺ ions are in higher concentrations outside of the cell, the concentration and voltage differences both drive them into the cell when Na⁺ channels open. Depolarization opens both the sodium and potassium channels in the membrane, allowing the ions to flow into and out of the axon, respectively. If the depolarization is small （say, increasing ''V_m'' from −70&nbsp;mV to −60&nbsp;mV）, the outward potassium current overwhelms the inward sodium current and the membrane repolarizes back to its normal resting potential around −70&nbsp;mV.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfn|Junge|1981|pp=89–90}}{{sfn|Schmidt-Nielsen|1997|p=484}} However, if the depolarization is large enough, the inward sodium current increases more than the outward potassium current and a runaway condition （[[positive feedback]]） results: the more inward current there is, the more ''V_m'' increases, which in turn further increases the inward current.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=48–49|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2p=141|3a1=Schmidt-Nielsen|3y=1997|3p=483|4a1=Junge|4y=1981|4p=89}} A sufficiently strong depolarization （increase in ''V_m''） causes the voltage-sensitive sodium channels to open; the increasing permeability to sodium drives ''V_m'' closer to the sodium equilibrium voltage ''E''_Na≈ +55&nbsp;mV. The increasing voltage in turn causes even more sodium channels to open, which pushes ''V_m'' still further towards ''E''_Na. This positive feedback continues until the sodium channels are fully open and ''V_m'' is close to ''E''_Na.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfn|Junge|1981|pp=89–90}}{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=49–50|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2pp=140–141|3a1=Schmidt-Nielsen|3y=1997|3pp=480–481}}{{sfn|Schmidt-Nielsen|1997|pp=483–484}} The sharp rise in ''V_m'' and sodium permeability correspond to the ''rising phase'' of the action potential.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfn|Junge|1981|pp=89–90}}{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=49–50|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2pp=140–141|3a1=Schmidt-Nielsen|3y=1997|3pp=480–481}}{{sfn|Schmidt-Nielsen|1997|pp=483–484}}

For a neuron at rest, there is a high concentration of sodium and chloride ions in the [[extracellular fluid]] compared to the [[intracellular fluid]], while there is a high concentration of potassium ions in the intracellular fluid compared to the extracellular fluid. The difference in concentrations, which causes ions to move [[Second law of thermodynamics|from a high to a low concentration]], and electrostatic effects （attraction of opposite charges） are responsible for the movement of ions in and out of the neuron. The inside of a neuron has a negative charge, relative to the cell exterior, from the movement of K⁺ out of the cell. The neuron membrane is more permeable to K⁺ than to other ions, allowing this ion to selectively move out of the cell, down its concentration gradient. This concentration gradient along with [[potassium leak channel]]s present on the membrane of the neuron causes an [[wikt:Special:Search/efflux|efflux]] of potassium ions making the resting potential close to ''E''_K&nbsp;≈&nbsp;–75&nbsp;mV.{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1p=34|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2p=134|3a1=Schmidt-Nielsen|3y=1997|3pp=478–480}} Since Na⁺ ions are in higher concentrations outside of the cell, the concentration and voltage differences both drive them into the cell when Na⁺ channels open. Depolarization opens both the sodium and potassium channels in the membrane, allowing the ions to flow into and out of the axon, respectively. If the depolarization is small （say, increasing ''V_m'' from −70&nbsp;mV to −60&nbsp;mV）, the outward potassium current overwhelms the inward sodium current and the membrane repolarizes back to its normal resting potential around −70&nbsp;mV.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfn|Junge|1981|pp=89–90}}{{sfn|Schmidt-Nielsen|1997|p=484}} However, if the depolarization is large enough, the inward sodium current increases more than the outward potassium current and a runaway condition （[[positive feedback]]） results: the more inward current there is, the more ''V_m'' increases, which in turn further increases the inward current.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=48–49|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2p=141|3a1=Schmidt-Nielsen|3y=1997|3p=483|4a1=Junge|4y=1981|4p=89}} A sufficiently strong depolarization （increase in ''V_m''） causes the voltage-sensitive sodium channels to open; the increasing permeability to sodium drives ''V_m'' closer to the sodium equilibrium voltage ''E''_Na≈ +55&nbsp;mV. The increasing voltage in turn causes even more sodium channels to open, which pushes ''V_m'' still further towards ''E''_Na. This positive feedback continues until the sodium channels are fully open and ''V_m'' is close to ''E''_Na.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfn|Junge|1981|pp=89–90}}{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=49–50|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2pp=140–141|3a1=Schmidt-Nielsen|3y=1997|3pp=480–481}}{{sfn|Schmidt-Nielsen|1997|pp=483–484}} The sharp rise in ''V_m'' and sodium permeability correspond to the ''rising phase'' of the action potential.{{sfn|Bullock|Orkand|Grinnell|1977|pp=150–151}}{{sfn|Junge|1981|pp=89–90}}{{sfnm|1a1=Purves|1a2=Augustine|1a3=Fitzpatrick|1a4=Hall|1y=2008|1pp=49–50|2a1=Bullock|2a2=Orkand|2a3=Grinnell|2y=1977|2pp=140–141|3a1=Schmidt-Nielsen|3y=1997|3pp=480–481}}{{sfn|Schmidt-Nielsen|1997|pp=483–484}}

 

对于处于静息状态的神经元来说，细胞外液中的钠离子和氯离子浓度高于细胞内液，而细胞内液中的钾离子浓度高于细胞外液。导致离子从高浓度移动到低浓度的浓度差，以及静电效应（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。

 

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

The critical threshold voltage for this runaway condition is usually around −45&nbsp;mV, but it depends on the recent activity of the axon. A cell that has just fired an action potential cannot fire another one immediately, since the Na⁺ channels have not recovered from the inactivated state. The period during which no new action potential can be fired is called the ''absolute refractory period''.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|p=49}}{{sfn|Stevens|1966|pp=19–20}}{{sfnm|1a1=Bullock|1a2=Orkand|1a3=Grinnell|1y=1977|1p=151|2a1=Junge|2y=1981|2pp=4–5}} At longer times, after some but not all of the ion channels have recovered, the axon can be stimulated to produce another action potential, but with a higher threshold, requiring a much stronger depolarization, e.g., to −30&nbsp;mV. The period during which action potentials are unusually difficult to evoke is called the ''relative refractory period''.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|p=49}}{{sfn|Stevens|1966|pp=19–20}}{{sfnm|1a1=Bullock|1a2=Orkand|1a3=Grinnell|1y=1977|1p=151|2a1=Junge|2y=1981|2pp=4–5}}

The critical threshold voltage for this runaway condition is usually around −45&nbsp;mV, but it depends on the recent activity of the axon. A cell that has just fired an action potential cannot fire another one immediately, since the Na⁺ channels have not recovered from the inactivated state. The period during which no new action potential can be fired is called the ''absolute refractory period''.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|p=49}}{{sfn|Stevens|1966|pp=19–20}}{{sfnm|1a1=Bullock|1a2=Orkand|1a3=Grinnell|1y=1977|1p=151|2a1=Junge|2y=1981|2pp=4–5}} At longer times, after some but not all of the ion channels have recovered, the axon can be stimulated to produce another action potential, but with a higher threshold, requiring a much stronger depolarization, e.g., to −30&nbsp;mV. The period during which action potentials are unusually difficult to evoke is called the ''relative refractory period''.{{sfn|Purves|Augustine|Fitzpatrick|Hall|2008|p=49}}{{sfn|Stevens|1966|pp=19–20}}{{sfnm|1a1=Bullock|1a2=Orkand|1a3=Grinnell|1y=1977|1p=151|2a1=Junge|2y=1981|2pp=4–5}}

The positive feedback of the rising phase slows and comes to a halt as the sodium ion channels become maximally open. At the peak of the action potential, the sodium permeability is maximized and the membrane voltage ''V_m'' is nearly equal to the sodium equilibrium voltage ''E''_Na. However, the same raised voltage that opened the sodium channels initially also slowly shuts them off, by closing their pores; the sodium channels become ''inactivated''.{{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 ''V_m'' 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 ''V_m'' 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}}

The positive feedback of the rising phase slows and comes to a halt as the sodium ion channels become maximally open. At the peak of the action potential, the sodium permeability is maximized and the membrane voltage ''V_m'' is nearly equal to the sodium equilibrium voltage ''E''_Na. However, the same raised voltage that opened the sodium channels initially also slowly shuts them off, by closing their pores; the sodium channels become ''inactivated''.{{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 ''V_m'' 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 ''V_m'' 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}}

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

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”。

 

===后超极化===

===Afterhyperpolarization===

The depolarized voltage opens additional voltage-dependent potassium channels, and some of these do not close right away when the membrane returns to its normal resting voltage. In addition, [[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 ''V_m'' even closer to the potassium equilibrium voltage ''E''_K. The membrane potential goes below the resting membrane potential. Hence, there is an undershoot or [[hyperpolarization (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}}

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 ''V_m'' even closer to the potassium equilibrium voltage ''E''_K. The membrane potential goes below the resting membrane potential. Hence, there is an undershoot or [[hyperpolarization (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}}

===Refractory period===

===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.

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.

= = = 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。

<nowiki>= = =</nowiki>

 

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.

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.

==Propagation==

==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 }}<br />* {{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>

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 }}<br />* {{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>

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" />< br/> *

 

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" />< br/> *  

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

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

一旦膜片上的一个动作电位发生了，膜片需要时间恢复才能再次激活。在分子水平上，这个绝对不应期（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。

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

===Myelin and saltatory conduction===

===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.

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.

 

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。

 

为了在神经系统中快速有效地传递电信号，某些神经元的轴突上覆盖着髓鞘。髓鞘是一种多层膜，它将轴突包裹在一段段中，这段段间隔被称为郎飞结。它是由专门的细胞产生的: 施万细胞专门在周围神经系统，少突胶质细胞专门在中枢神经系统。髓鞘减少膜电容和增加膜电阻在节间间隔，从而允许快速，跳跃性的动作电位从一个节点到另一个节点e.<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&nbsp;[[Metre per second|meter per second]] （m/s） to over 100&nbsp;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>

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&nbsp;[[Metre per second|meter per second]] （m/s） to over 100&nbsp;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>

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 }}<br />* {{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 }}<br />* {{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.

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 }}<br />* {{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 }}<br />* {{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.

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" />< br/> 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。

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" />< br/> 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。

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>

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>

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" />

[[File:Cable theory Neuron RC circuit v3.svg|thumb|300x300px|Cable theory's simplified view of a neuronal fiber. The connected [[RC circuit]]s correspond to adjacent segments of a passive [[neurite]]. The extracellular resistances ''r_e'' （the counterparts of the intracellular resistances ''r_i''） are not shown, since they are usually negligibly small; the extracellular medium may be assumed to have the same voltage everywhere.

电缆理论的神经原纤维的简化视野。连接的RC电路对应于被动的神经突相邻的分节。|链接=Special:FilePath/Cable_theory_Neuron_RC_circuit_v3.svg]]

[[File:Cable theory Neuron RC circuit v3.svg|thumb|300x300px|Cable theory's simplified view of a neuronal fiber. The connected [[RC circuit]]s correspond to adjacent segments of a passive [[neurite]]. The extracellular resistances ''r_e'' （the counterparts of the intracellular resistances ''r_i''） are not shown, since they are usually negligibly small; the extracellular medium may be assumed to have the same voltage everywhere.|链接=Special:FilePath/Cable_theory_Neuron_RC_circuit_v3.svg]]

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" />

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" />

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" />

 

轴突内电流的流动可以用电缆理论来定量描述<ref name="rall_1989" /> 。.<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" />

 

:<math>

:<math>

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

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

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>

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>

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" />。

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" />

 

[[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.|链接=Special:FilePath/Gap_cell_junction-en.svg]]

兴奋性细胞之间的电突触让离子直接从一个神经元到另一个细胞流动，比化学突触快得多。|链接=Special:FilePath/Gap_cell_junction-en.svg]]

===Electrical synapses===

===电突触Electrical synapses===

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]].

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]].

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。

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。

===Neuromuscular junctions===

===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>

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>

突触间隙的一个特例是神经肌肉接点，运动神经元的轴突终止于肌纤维上.<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" />。

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" />

==Other cell types 其他细胞类型==

==Other cell types 其他细胞类型==

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.

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.

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。

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。

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>

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>

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

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" />

===Muscular action potentials===

===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&nbsp;ms, the absolute refractory period is roughly 1–3&nbsp;ms, and the conduction velocity along the muscle is roughly 5&nbsp;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 />

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&nbsp;ms, the absolute refractory period is roughly 1–3&nbsp;ms, and the conduction velocity along the muscle is roughly 5&nbsp;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 />

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" />。

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" />

===Plant action potentials===

===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>

[[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>

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" />。

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" />

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

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

Some plants （e.g. ''[[Dionaea muscipula]]''） use sodium-gated channels to operate movements and essentially "count". ''Dionaea muscipula'', also known as the Venus flytrap, is found in subtropical wetlands in North and South Carolina.<ref name=":16">{{Cite journal|last=Luken|first=James O. | name-list-style = vanc |date= December 2005 |title=Habitats of Dionaea muscipula (Venus' Fly Trap), Droseraceae, Associated with Carolina Bays|journal=Southeastern Naturalist|language=en|volume=4|issue=4|pages=573–584|doi=10.1656/1528-7092(2005)004[0573:HODMVF]2.0.CO;2|issn=1528-7092}}</ref> When there are poor soil nutrients, the flytrap relies on a diet of insects and animals.<ref name=":1">{{cite journal | vauthors = Böhm J, Scherzer S, Krol E, Kreuzer I, von Meyer K, Lorey C, Mueller TD, Shabala L, Monte I, Solano R, Al-Rasheid KA, Rennenberg H, Shabala S, Neher E, Hedrich R | display-authors = 6 | title = The Venus Flytrap Dionaea muscipula Counts Prey-Induced Action Potentials to Induce Sodium Uptake | journal = Current Biology | volume = 26 | issue = 3 | pages = 286–95 | date = February 2016 | pmid = 26804557 | pmc = 4751343 | doi = 10.1016/j.cub.2015.11.057 }}</ref> Despite research on the plant, there lacks an understanding behind the molecular basis to the Venus flytraps, and carnivore plants in general.<ref name=":2">{{cite journal | vauthors = Hedrich R, Neher E | title = Venus Flytrap: How an Excitable, Carnivorous Plant Works | journal = Trends in Plant Science | volume = 23 | issue = 3 | pages = 220–234 | date = March 2018 | pmid = 29336976 | doi = 10.1016/j.tplants.2017.12.004 }}</ref>

Some plants （e.g. ''[[Dionaea muscipula]]''） use sodium-gated channels to operate movements and essentially "count". ''Dionaea muscipula'', also known as the Venus flytrap, is found in subtropical wetlands in North and South Carolina.<ref name=":16">{{Cite journal|last=Luken|first=James O. | name-list-style = vanc |date= December 2005 |title=Habitats of Dionaea muscipula (Venus' Fly Trap), Droseraceae, Associated with Carolina Bays|journal=Southeastern Naturalist|language=en|volume=4|issue=4|pages=573–584|doi=10.1656/1528-7092(2005)004[0573:HODMVF]2.0.CO;2|issn=1528-7092}}</ref> When there are poor soil nutrients, the flytrap relies on a diet of insects and animals.<ref name=":1">{{cite journal | vauthors = Böhm J, Scherzer S, Krol E, Kreuzer I, von Meyer K, Lorey C, Mueller TD, Shabala L, Monte I, Solano R, Al-Rasheid KA, Rennenberg H, Shabala S, Neher E, Hedrich R | display-authors = 6 | title = The Venus Flytrap Dionaea muscipula Counts Prey-Induced Action Potentials to Induce Sodium Uptake | journal = Current Biology | volume = 26 | issue = 3 | pages = 286–95 | date = February 2016 | pmid = 26804557 | pmc = 4751343 | doi = 10.1016/j.cub.2015.11.057 }}</ref> Despite research on the plant, there lacks an understanding behind the molecular basis to the Venus flytraps, and carnivore plants in general.<ref name=":2">{{cite journal | vauthors = Hedrich R, Neher E | title = Venus Flytrap: How an Excitable, Carnivorous Plant Works | journal = Trends in Plant Science | volume = 23 | issue = 3 | pages = 220–234 | date = March 2018 | pmid = 29336976 | doi = 10.1016/j.tplants.2017.12.004 }}</ref>

一些植物（例如:。捕蝇草）使用钠门控通道操作运动，本质上是“计数”。捕蝇草，也被称为捕蝇草，发现于北卡罗来纳州和南卡罗来纳州的亚热带湿地.<ref name=":16" />。当土壤养分不足时，捕蝇草依靠昆虫和动物为食.<ref name=":1" />。尽管对这种植物进行了研究，但对于金星捕蝇草和一般的食肉植物的分子基础还缺乏了解.<ref name=":2" />。

一些植物（例如:。捕蝇草）使用钠门控通道操作运动，本质上是“计数”。捕蝇草，也被称为捕蝇草，发现于北卡罗来纳州和南卡罗来纳州的亚热带湿地。<ref name=":16" /> 当土壤养分不足时，捕蝇草依靠昆虫和动物为食。<ref name=":1" />。尽管对这种植物进行了研究，但对于金星捕蝇草和一般的食肉植物的分子基础还缺乏了解。<ref name=":2" />

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.

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.

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/]   

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/]   

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" />

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" />

然而，捕蝇器不会在一次触发后关闭。相反，它需要激活2根或更多的毛发.<ref name=":1" /><ref name=":2" /> 。如果只有一根头发被触发，它就会将这个激活作为一个假阳性而抛出。此外，第二根头发必须在一定的时间间隔（0.75 s-40 s）内被激活，才能在第一次激活中注册.<ref name=":2" /> 。因此，钙的积累开始并且从第一个触发点开始慢慢下降。当第二个动作电位在时间间隔内被激发时，它达到钙阈值使细胞去极化，在几分之一秒内关闭捕获物的陷阱.<ref name=":2" /> 。

然而，捕蝇器不会在一次触发后关闭。相反，它需要激活2根或更多的毛发。<ref name=":1" /><ref name=":2" /> 如果只有一根头发被触发，它就会将这个激活作为一个假阳性而抛出。此外，第二根头发必须在一定的时间间隔（0.75 s-40 s）内被激活，才能在第一次激活中注册。<ref name=":2" /> 因此，钙的积累开始并且从第一个触发点开始慢慢下降。当第二个动作电位在时间间隔内被激发时，它达到钙阈值使细胞去极化，在几分之一秒内关闭捕获物的陷阱。<ref name=":2" />

Together with the subsequent release of positive potassium ions the action potential in plants involves an [[osmotic]] loss of salt （KCl）. Whereas, the animal action potential is osmotically neutral because equal amounts of entering sodium and leaving potassium cancel each other osmotically. The interaction of electrical and osmotic relations in plant cells<ref name="Gradmann_1998" group="lower-alpha">{{cite journal | vauthors = Gradmann D, Hoffstadt J | title = Electrocoupling of ion transporters in plants: interaction with internal ion concentrations | journal = The Journal of Membrane Biology | volume = 166 | issue = 1 | pages = 51–9 | date = November 1998 | pmid = 9784585 | doi = 10.1007/s002329900446 | s2cid = 24190001 }}</ref> appears to have arisen from an osmotic function of electrical excitability in a common unicellular ancestors of plants and animals under changing salinity conditions. Further, the present function of rapid signal transmission is seen as a newer accomplishment of [[metazoan]] cells in a more stable osmotic environment.<ref name="Gradmann_1980">

Together with the subsequent release of positive potassium ions the action potential in plants involves an [[osmotic]] loss of salt （KCl）. Whereas, the animal action potential is osmotically neutral because equal amounts of entering sodium and leaving potassium cancel each other osmotically. The interaction of electrical and osmotic relations in plant cells<ref name="Gradmann_1998" group="lower-alpha">{{cite journal | vauthors = Gradmann D, Hoffstadt J | title = Electrocoupling of ion transporters in plants: interaction with internal ion concentrations | journal = The Journal of Membrane Biology | volume = 166 | issue = 1 | pages = 51–9 | date = November 1998 | pmid = 9784585 | doi = 10.1007/s002329900446 | s2cid = 24190001 }}</ref> appears to have arisen from an osmotic function of electrical excitability in a common unicellular ancestors of plants and animals under changing salinity conditions. Further, the present function of rapid signal transmission is seen as a newer accomplishment of [[metazoan]] cells in a more stable osmotic environment.<ref name="Gradmann_1980">

Gradmann, D; Mummert, H in {{harvnb|Spanswick|Lucas|Dainty|1980|loc=''Plant action potentials'', pp. 333–344.}}</ref> It is likely that the familiar signaling function of action potentials in some vascular plants （e.g. ''[[Mimosa pudica]]''） arose independently from that in metazoan excitable cells.

Gradmann, D; Mummert, H in {{harvnb|Spanswick|Lucas|Dainty|1980|loc=''Plant action potentials'', pp. 333–344.}}</ref> It is likely that the familiar signaling function of action potentials in some vascular plants （e.g. ''[[Mimosa pudica]]''） arose independently from that in metazoan excitable cells.

随着随后释放的阳性钾离子，动作电位在植物中涉及盐（KCl）渗透损失。然而，动物的动作电位是渗透中性的，因为等量的钠进入和钾离开相互抵消渗透。植物细胞s<ref name="Gradmann_1998" group="lower-alpha" />中电和渗透关系的相互作用似乎起源于盐度变化条件下动植物共同的单细胞祖先的电兴奋渗透作用。此外，目前的快速信号传递功能被认为是后生动物细胞在更稳定的渗透环境中更新的成就.<ref name="Gradmann_1980" /> 。在一些维管植物中，动作电位的常见信号功能可能是。含羞草（Mimosa putica）是独立于后生动物兴奋细胞而产生的。

随着随后释放的阳性钾离子，动作电位在植物中涉及盐（KCl）渗透损失。然而，动物的动作电位是渗透中性的，因为等量的钠进入和钾离开相互抵消渗透。植物细胞<ref name="Gradmann_1998" group="lower-alpha" />中电和渗透关系的相互作用似乎起源于盐度变化条件下动植物共同的单细胞祖先的电兴奋渗透作用。此外，目前的快速信号传递功能被认为是后生动物细胞在更稳定的渗透环境中更新的成就.<ref name="Gradmann_1980" /> 。在一些维管植物中，动作电位的常见信号功能可能是。含羞草（Mimosa putica）是独立于后生动物兴奋细胞而产生的。

Unlike the rising phase and peak, the falling phase and after-hyperpolarization seem to depend primarily on cations that are not calcium. To initiate repolarization, the cell requires movement of potassium out of the cell through passive transportation on the membrane. This differs from neurons because the movement of potassium does not dominate the decrease in membrane potential; In fact, to fully repolarize, a plant cell requires energy in the form of ATP to assist in the release of hydrogen from the cell – utilizing a transporter commonly known as H+-ATPase.<ref name="Opritov">Opritov, V A, et al. “Direct Coupling of Action Potential Generation in Cells of a Higher Plant (Cucurbita Pepo) with the Operation of an Electrogenic Pump.” ''Russian Journal of Plant Physiology'', vol. 49, no. 1, 2002, pp. 142–147.</ref><ref name=":2" />

Unlike the rising phase and peak, the falling phase and after-hyperpolarization seem to depend primarily on cations that are not calcium. To initiate repolarization, the cell requires movement of potassium out of the cell through passive transportation on the membrane. This differs from neurons because the movement of potassium does not dominate the decrease in membrane potential; In fact, to fully repolarize, a plant cell requires energy in the form of ATP to assist in the release of hydrogen from the cell – utilizing a transporter commonly known as H+-ATPase.<ref name="Opritov">Opritov, V A, et al. “Direct Coupling of Action Potential Generation in Cells of a Higher Plant (Cucurbita Pepo) with the Operation of an Electrogenic Pump.” ''Russian Journal of Plant Physiology'', vol. 49, no. 1, 2002, pp. 142–147.</ref><ref name=":2" />

不同于上升相和峰值，下降相和后超极化似乎主要依赖于不是钙的阳离子。为了启动复极化，细胞需要钾离子通过细胞膜上的被动运输离开细胞。事实上，为了完全再极化，植物细胞需要能量以 ATP 的形式帮助细胞释放氢-利用一种通常被称为 h +-ATP 酶的转运蛋白。奥普里托夫，v a，等。高等植物细胞动作电位的直接耦合与电生泵的运作俄罗斯植物生理学杂志，第一卷。49，不。1,2002，pp.142–147..<ref name="Opritov" /><ref name=":2" />

不同于上升相和峰值，下降相和后超极化似乎主要依赖于不是钙的阳离子。为了启动复极化，细胞需要钾离子通过细胞膜上的被动运输离开细胞。事实上，为了完全再极化，植物细胞需要能量以 ATP 的形式帮助细胞释放氢-利用一种通常被称为 H+-ATPase 酶的转运蛋白。<ref name="Opritov" /><ref name=":2" />

 

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

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

Action potentials are found throughout [[multicellular organism]]s, including [[plant]]s, [[invertebrate]]s such as [[insect]]s, and [[vertebrate]]s such as [[reptile]]s and [[mammal]]s.<ref name="Fromm" group="lower-alpha">{{cite journal | vauthors = Fromm J, Lautner S | title = Electrical signals and their physiological significance in plants | journal = Plant, Cell & Environment | volume = 30 | issue = 3 | pages = 249–257 | date = March 2007 | pmid = 17263772 | doi = 10.1111/j.1365-3040.2006.01614.x }}</ref> [[Sponge]]s seem to be the main [[phylum]] of multicellular [[eukaryote]]s that does not transmit action potentials, although some studies have suggested that these organisms have a form of electrical signaling, too.<ref group="lower-alpha" name=":15">{{cite journal | vauthors = Leys SP, Mackie GO, Meech RW | title = Impulse conduction in a sponge | journal = The Journal of Experimental Biology | volume = 202 (Pt 9) | issue = 9 | pages = 1139–50 | date = May 1999 | doi = 10.1242/jeb.202.9.1139 | pmid = 10101111 | url = http://jeb.biologists.org/cgi/pmidlookup?view=long&pmid=10101111 }}</ref> The resting potential, as well as the size and duration of the action potential, have not varied much with evolution, although the [[conduction velocity]] does vary dramatically with axonal diameter and myelination.

Action potentials are found throughout [[multicellular organism]]s, including [[plant]]s, [[invertebrate]]s such as [[insect]]s, and [[vertebrate]]s such as [[reptile]]s and [[mammal]]s.<ref name="Fromm" group="lower-alpha">{{cite journal | vauthors = Fromm J, Lautner S | title = Electrical signals and their physiological significance in plants | journal = Plant, Cell & Environment | volume = 30 | issue = 3 | pages = 249–257 | date = March 2007 | pmid = 17263772 | doi = 10.1111/j.1365-3040.2006.01614.x }}</ref> [[Sponge]]s seem to be the main [[phylum]] of multicellular [[eukaryote]]s that does not transmit action potentials, although some studies have suggested that these organisms have a form of electrical signaling, too.<ref group="lower-alpha" name=":15">{{cite journal | vauthors = Leys SP, Mackie GO, Meech RW | title = Impulse conduction in a sponge | journal = The Journal of Experimental Biology | volume = 202 (Pt 9) | issue = 9 | pages = 1139–50 | date = May 1999 | doi = 10.1242/jeb.202.9.1139 | pmid = 10101111 | url = http://jeb.biologists.org/cgi/pmidlookup?view=long&pmid=10101111 }}</ref> The resting potential, as well as the size and duration of the action potential, have not varied much with evolution, although the [[conduction velocity]] does vary dramatically with axonal diameter and myelination.

在多细胞生物，包括植物、无脊椎动物如昆虫和脊椎动物如爬行动物和哺乳动物中发现了动作电位.<ref name="Fromm" group="lower-alpha" />。海绵似乎是不传递动作电位的多细胞真核生物的主要门类，尽管一些研究表明这些生物也有一种电信号的形式.<ref name=":15" group="lower-alpha" /> 。虽然神经传导速度随轴突直径和髓鞘形成而发生显著变化，但神经静息电位和动作电位的大小和持续时间并没有随着进化而发生很大变化。

在多细胞生物，包括植物、无脊椎动物如昆虫和脊椎动物如爬行动物和哺乳动物中发现了动作电位。<ref name="Fromm" group="lower-alpha" /> 海绵似乎是不传递动作电位的多细胞真核生物的主要门类，尽管一些研究表明这些生物也有一种电信号的形式。<ref name=":15" group="lower-alpha" /> 虽然神经传导速度随轴突直径和髓鞘形成而发生显著变化，但神经静息电位和动作电位的大小和持续时间并没有随着进化而发生很大变化。

{| class="wikitable" id="action_potential_texonomic_comparison" border="2" cellpadding="5" cellspacing="1" align="center"

{| class="wikitable" id="action_potential_texonomic_comparison" border="2" cellpadding="5" cellspacing="1" align="center"

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>

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>

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

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

==Experimental methods==

==实验方法Experimental methods==

[[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]]

[[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]]

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.

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.

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。

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&nbsp;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.

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&nbsp;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.

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e.<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。

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。

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 ''I_C'' 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 ''V_m'', the solution was to design a circuit that kept ''V_m'' fixed （zero rate of change） regardless of the currents flowing across the membrane. Thus, the current required to keep ''V_m'' at a fixed value is a direct reflection of the current flowing through the membrane. Other electronic advances included the use of [[Faraday cage]]s and electronics with high [[input impedance]], so that the measurement itself did not affect the voltage being measured.{{sfn|Kettenmann|Grantyn|1992}}

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 ''I_C'' 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 ''V_m'', the solution was to design a circuit that kept ''V_m'' fixed （zero rate of change） regardless of the currents flowing across the membrane. Thus, the current required to keep ''V_m'' at a fixed value is a direct reflection of the current flowing through the membrane. Other electronic advances included the use of [[Faraday cage]]s and electronics with high [[input impedance]], so that the measurement itself did not affect the voltage being measured.{{sfn|Kettenmann|Grantyn|1992}}

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 }}<br />* {{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>

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 }}<br />* {{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>

   

   

 

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

第三个问题是如何获得足够小的电极来记录单个轴突内的电压而不对其造成干扰，这个问题在1949年由于玻璃微移液管电极,<ref name="ling_1949" group="lower-alpha" /> 的发明而得到解决，并且很快被其他研究人员采用.<ref name="nastuk_1950" group="lower-alpha" /><ref name="brock_1952" group="lower-alpha" /> 。这种方法的改进可以生产出100纳米的电极尖端，同时也提供了高的输入阻抗.<ref name=":20" /> 。动作电位中的 Snell 和 FM 也可以用放置在神经元旁的小金属电极记录下来，用含有 eosfet 的神经芯片，或者用对 Ca < sup > 2 + 或电压敏感的染料记录下来。.<ref name="dyes" group="lower-alpha" />< br/> *

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

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

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

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

玻璃微吸管电极测量通过许多离子通道的电流总和，研究单个离子通道的电学性质在20世纪70年代埃尔温 · 内尔和伯特 · 萨克曼发明的膜片钳成为可能。由于这一发现，他们在1991年被授予诺贝尔生理学或医学奖科学奖.<ref name="Nobel_1991" group="lower-Greek" />。膜片钳技术证实了离子通道具有分立的电导状态，如开放状态、闭合状态和失活状态。

玻璃微吸管电极测量通过许多离子通道的电流总和，研究单个离子通道的电学性质在 20 世纪 70 年代 [[Erwin Neher]] and [[Bert Sakmann]].埃尔温 · 内尔和伯特 · 萨克曼发明的膜片钳（patch clamp）成为可能。由于这一发现，他们在1991年被授予诺贝尔生理学或医学奖科学奖。<ref name="Nobel_1991" group="lower-Greek" /> 膜片钳技术证实了离子通道具有分立的电导状态，如开放状态、闭合状态和失活状态。

[[Optical imaging]] technologies have been developed in recent years to measure action potentials, either via simultaneous multisite recordings or with ultra-spatial resolution. Using [[Potentiometric dyes|voltage-sensitive dyes]], action potentials have been optically recorded from a tiny patch of [[cardiomyocyte]] membrane.<ref name="pmid19289075" group="lower-alpha">{{cite journal | vauthors = Bu G, Adams H, Berbari EJ, Rubart M | title = Uniform action potential repolarization within the sarcolemma of in situ ventricular cardiomyocytes | journal = Biophysical Journal | volume = 96 | issue = 6 | pages = 2532–46 | date = March 2009 | pmid = 19289075 | pmc = 2907679 | doi = 10.1016/j.bpj.2008.12.3896 | bibcode = 2009BpJ....96.2532B }}</ref>

[[Optical imaging]] technologies have been developed in recent years to measure action potentials, either via simultaneous multisite recordings or with ultra-spatial resolution. Using [[Potentiometric dyes|voltage-sensitive dyes]], action potentials have been optically recorded from a tiny patch of [[cardiomyocyte]] membrane.<ref name="pmid19289075" group="lower-alpha">{{cite journal | vauthors = Bu G, Adams H, Berbari EJ, Rubart M | title = Uniform action potential repolarization within the sarcolemma of in situ ventricular cardiomyocytes | journal = Biophysical Journal | volume = 96 | issue = 6 | pages = 2532–46 | date = March 2009 | pmid = 19289075 | pmc = 2907679 | doi = 10.1016/j.bpj.2008.12.3896 | bibcode = 2009BpJ....96.2532B }}</ref>

近年来发展了光学成像技术，通过同时多点记录或超空间分辨率来测量动作电位。利用电压敏感染料，从一小块心肌细胞膜上记录了动作电位.<ref name="pmid19289075" group="lower-alpha" />。

近年来发展了光学成像技术，通过同时多点记录或超空间分辨率来测量动作电位。利用电压敏感染料，从一小块心肌细胞膜上记录了动作电位。<ref name="pmid19289075" group="lower-alpha" />

==Neurotoxins==

==神经毒素Neurotoxins==

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

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

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" />。

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" />。

==Quantitative models==

==定量模型Quantitative models==

[[Image:MembraneCircuit.svg|thumb|336px|right|Equivalent electrical circuit for the Hodgkin–Huxley model of the action potential. ''I_m'' and ''V_m'' represent the current through, and the voltage across, a small patch of membrane, respectively. The ''C_m'' represents the capacitance of the membrane patch, whereas the four ''g'''s represent the [[electrical conductance|conductances]] of four types of ions. The two conductances on the left, for potassium （K） and sodium （Na）, are shown with arrows to indicate that they can vary with the applied voltage, corresponding to the [[voltage-gated ion channel|voltage-sensitive ion channels]]. The two conductances on the right help determine the [[resting membrane potential]].

[[Image:MembraneCircuit.svg|thumb|336px|right|Equivalent electrical circuit for the Hodgkin–Huxley model of the action potential. ''I_m'' and ''V_m'' represent the current through, and the voltage across, a small patch of membrane, respectively. The ''C_m'' represents the capacitance of the membrane patch, whereas the four ''g'''s represent the [[electrical conductance|conductances]] of four types of ions. The two conductances on the left, for potassium （K） and sodium （Na）, are shown with arrows to indicate that they can vary with the applied voltage, corresponding to the [[voltage-gated ion channel|voltage-sensitive ion channels]]. The two conductances on the right help determine the [[resting membrane potential]].