更改

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

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

[[File:Membrane Permeability of a Neuron During an Action Potential.svg|thumb|upright=1.75|right|Ion movement during an action potential.<br />''Key:'' a） Sodium （Na⁺） ion. b） Potassium （K⁺） ion. c） Sodium channel. d） Potassium channel. e） Sodium-potassium pump.<br/> In the stages of an action potential, the permeability of the membrane of the neuron changes. At the '''resting state''' （1）, sodium and potassium ions have limited ability to pass through the membrane, and the neuron has a net negative charge inside. Once the action potential is triggered, the '''depolarization''' （2） of the neuron activates sodium channels, allowing sodium ions to pass through the cell membrane into the cell, resulting in a net positive charge in the neuron relative to the extracellular fluid. After the action potential peak is reached, the neuron begins '''repolarization''' （3）, where the sodium channels close and potassium channels open, allowing potassium ions to cross the membrane into the extracellular fluid, returning the membrane potential to a negative value. Finally, there is a '''refractory period''' （4）, during which the voltage-dependent ion channels are [[Voltage-gated ion channel#Mechanism|inactivated]] while the Na⁺ and K⁺ ions return to their resting state distributions across the membrane （1）, and the neuron is ready to repeat the process for the next action potential.

[[File:Membrane Permeability of a Neuron During an Action Potential.svg|thumb|upright=1.75|right|动作电位过程中的离子移动。图注：a）钠离子（Na⁺）、b）钾离子（K⁺）、c） 钠通道、d）钾通道、e）钠钾泵。

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

 

 

在动作电位发生的过程中，神经元质膜的通透性发生变化。在'''静息状态'''（1）下，钠离子和钾离子通过膜的能力有限，神经元内部具有净负电荷。一旦触发动作电位，神经元的'''去极化'''（2）激活钠通道，允许钠离子通过细胞膜进入细胞，导致神经元相对于细胞外液的净正电荷。达到动作电位峰值后，神经元开始'''复极化'''（3），其中钠通道关闭，钾通道打开，允许钾离子穿过膜进入细胞外液，使膜电位恢复为负值。最后，有一个'''不应期'''（4），在此期间，电压依赖性离子通道失活，而Na ⁺和K ⁺离子返回到其在膜上的静息状态分布（1），并且神经元准备重复该过程产生下一个动作电位。|链接=Special:FilePath/Membrane_Permeability_of_a_Neuron_During_an_Action_Potential.svg]]

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

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

Neurons are electrically excitable cells composed, in general, of one or more dendrites, a single [[soma (biology)|soma]], a single axon and one or more [[axon terminal]]s. Dendrites are cellular projections whose primary function is to receive synaptic signals. Their protrusions, known as [[dendritic spine]]s, are designed to capture the neurotransmitters released by the presynaptic neuron. They have a high concentration of [[ligand-gated ion channel]]s. These spines have a thin neck connecting a bulbous protrusion to the dendrite. This ensures that changes occurring inside the spine are less likely to affect the neighboring spines. The dendritic spine can, with rare exception （see [[Long-term potentiation#Properties|LTP]]）, act as an independent unit. The dendrites extend from the soma, which houses the [[Cell nucleus|nucleus]], and many of the "normal" [[eukaryote|eukaryotic]] organelles. Unlike the spines, the surface of the soma is populated by voltage activated ion channels. These channels help transmit the signals generated by the dendrites. Emerging out from the soma is the [[axon hillock]]. This region is characterized by having a very high concentration of voltage-activated sodium channels. In general, it is considered to be the spike initiation zone for action potentials, i.e. the [[trigger zone]]. Multiple signals generated at the spines, and transmitted by the soma all converge here. Immediately after the axon hillock is the axon. This is a thin tubular protrusion traveling away from the soma. The axon is insulated by a [[myelin]] sheath. Myelin is composed of either [[Schwann cells]] （in the peripheral nervous system） or [[oligodendrocytes]] （in the central nervous system）, both of which are types of [[glial cells]]. Although glial cells are not involved with the transmission of electrical signals, they communicate and provide important biochemical support to neurons. To be specific, myelin wraps multiple times around the axonal segment, forming a thick fatty layer that prevents ions from entering or escaping the axon. This insulation prevents significant signal decay as well as ensuring faster signal speed. This insulation, however, has the restriction that no channels can be present on the surface of the axon. There are, therefore, regularly spaced patches of membrane, which have no insulation. These [[nodes of Ranvier]] can be considered to be "mini axon hillocks", as their purpose is to boost the signal in order to prevent significant signal decay. At the furthest end, the axon loses its insulation and begins to branch into several [[axon terminal]]s. These presynaptic terminals, or synaptic boutons, are a specialized area within the axon of the presynaptic cell that contains [[neurotransmitters]] enclosed in small membrane-bound spheres called [[synaptic vesicle]]s.

Neurons are electrically excitable cells composed, in general, of one or more dendrites, a single [[soma (biology)|soma]], a single axon and one or more [[axon terminal]]s. Dendrites are cellular projections whose primary function is to receive synaptic signals. Their protrusions, known as [[dendritic spine]]s, are designed to capture the neurotransmitters released by the presynaptic neuron. They have a high concentration of [[ligand-gated ion channel]]s. These spines have a thin neck connecting a bulbous protrusion to the dendrite. This ensures that changes occurring inside the spine are less likely to affect the neighboring spines. The dendritic spine can, with rare exception （see [[Long-term potentiation#Properties|LTP]]）, act as an independent unit. The dendrites extend from the soma, which houses the [[Cell nucleus|nucleus]], and many of the "normal" [[eukaryote|eukaryotic]] organelles. Unlike the spines, the surface of the soma is populated by voltage activated ion channels. These channels help transmit the signals generated by the dendrites. Emerging out from the soma is the [[axon hillock]]. This region is characterized by having a very high concentration of voltage-activated sodium channels. In general, it is considered to be the spike initiation zone for action potentials, i.e. the [[trigger zone]]. Multiple signals generated at the spines, and transmitted by the soma all converge here. Immediately after the axon hillock is the axon. This is a thin tubular protrusion traveling away from the soma. The axon is insulated by a [[myelin]] sheath. Myelin is composed of either [[Schwann cells]] （in the peripheral nervous system） or [[oligodendrocytes]] （in the central nervous system）, both of which are types of [[glial cells]]. Although glial cells are not involved with the transmission of electrical signals, they communicate and provide important biochemical support to neurons. To be specific, myelin wraps multiple times around the axonal segment, forming a thick fatty layer that prevents ions from entering or escaping the axon. This insulation prevents significant signal decay as well as ensuring faster signal speed. This insulation, however, has the restriction that no channels can be present on the surface of the axon. There are, therefore, regularly spaced patches of membrane, which have no insulation. These [[nodes of Ranvier]] can be considered to be "mini axon hillocks", as their purpose is to boost the signal in order to prevent significant signal decay. At the furthest end, the axon loses its insulation and begins to branch into several [[axon terminal]]s. These presynaptic terminals, or synaptic boutons, are a specialized area within the axon of the presynaptic cell that contains [[neurotransmitters]] enclosed in small membrane-bound spheres called [[synaptic vesicle]]s.

===Initiation===

===Initiation===

[[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.

当动作电位到达突触前轴突（上）的末端时，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）。这些输入的兴奋性和抑制性突触后电位的组合可以在突触后神经元中开始新的动作电位。|链接=Special:FilePath/SynapseSchematic_en.svg]]

当动作电位到达突触前轴突（上部）的末端时，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）。这些输入的兴奋性和抑制性突触后电位的组合可以在突触后神经元中开始新的动作电位。|链接=Special:FilePath/SynapseSchematic_en.svg]]

在考虑动作电位沿轴突的传播及其在突触结节的终止之前，有必要考虑一下在轴突突起处引发动作电位的方法。最基本的要求就是把轴丘上的膜电位抬高到发放的域值以上。有几种方式可以发生这种去极化。

在考虑动作电位沿轴突的传播及其在突触结节的终止之前，有必要考虑一下在轴突突起处引发动作电位的方法。最基本的要求就是把轴丘上的膜电位抬高到发放的域值以上。有几种方式可以发生这种去极化。

在感觉神经元中，外部信号如压力、温度、光或声音与离子通道的开启和关闭相耦合，这反过来又改变了膜的离子通透性及其电压。这些电压变化可以是兴奋性（去极化）或抑制性（超极化），在某些感觉神经元中，它们的联合作用可以使轴突丘去极化，足以激发动作电位。人类的一些例子包括嗅觉受器神经元和迈斯纳氏小体，它们分别对嗅觉和触觉至关重要。然而，并不是所有的感觉神经元都将外部信号转换成动作电位，有些甚至没有轴突。相反，他们可以将信号转换成一种神经递质的释放，或者转换成连续分级的电位，这两种电位都可以刺激后续的神经元发出动作电位。例如，在人耳中，毛细胞将传入的声音转换成机械门控离子通道的开闭，这可能导致神经递质分子的释放。同样，在人类视网膜中，最初的感光细胞和下一层细胞（包括双极细胞和水平细胞）不产生动作电位，只有一些无长突细胞和第三层神经节细胞产生动作电位，然后动作电位沿视神经传递。

在感觉神经元中，外部信号如压力、温度、光或声音与离子通道的开启和关闭相耦合，这反过来又改变了膜的离子通透性及其电压。这些电压变化可以是兴奋性（去极化）或抑制性（超极化），在某些感觉神经元中，它们的联合作用可以使轴突丘去极化，足以激发动作电位。人类的一些例子包括嗅觉受器神经元和迈斯纳氏小体，它们分别对嗅觉和触觉至关重要。然而，并不是所有的感觉神经元都将外部信号转换成动作电位，有些甚至没有轴突。相反，他们可以将信号转换成一种神经递质的释放，或者转换成连续分级的电位，这两种电位都可以刺激后续的神经元发出动作电位。例如，在人耳中，毛细胞将传入的声音转换成机械门控离子通道的开闭，这可能导致神经递质分子的释放。同样，在人类视网膜中，最初的感光细胞和下一层细胞（包括双极细胞和水平细胞）不产生动作电位，只有一些无长突细胞和第三层神经节细胞产生动作电位，然后动作电位沿视神经传递。

===Pacemaker potentials 节拍器电位===

===Pacemaker potentials 起搏电位===

{{Main|Pacemaker potential}}

{{Main|Pacemaker potential}}

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

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

在 起搏器电位s中，细胞自发地去极化（具有向上斜率的直线），直到它发射动作电位。]]

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

In sensory neurons, action potentials result from an external stimulus. However, some excitable cells require no such stimulus to fire: They spontaneously depolarize their axon hillock and fire action potentials at a regular rate, like an internal clock. The voltage traces of such cells are known as [[pacemaker 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]].

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毛孔而慢慢关闭它们; 钠离子通道变得不活跃。这降低了细胞膜相对于钾离子的钠离子通透性，使膜电位重新回到静息值。同时，升高的电压开启了电压敏感性钾离子通道，膜钾离子通透性的增加促使 Vm 向 EK 方向运动。这些钠和钾通透性的变化使 Vm 迅速下降，使膜再极化，产生动作电位的“下降相”。

===<!--"Afterhyperpolarization" is a single word; please do not divide it into two words!-->Afterhyperpolarization===

===<!--"Afterhyperpolarization" is a single word; please do not divide it into two words!-->===

===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}}

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" />

= = = = 电缆理论 = = = 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" />

<nowiki>= = = = 电缆理论 = = =</nowiki>

 

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" />

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