更改

The term ''dendrites'' was first used in 1889 by [[Wilhelm His, Sr.|Wilhelm His]] to describe the number of smaller "protoplasmic processes" that were attached to a [[Neuron|nerve cell]].<ref>{{Cite book|title=Origins of neuroscience : a history of explorations into brain function|last=Finger|first=Stanley|publisher=Oxford University Press|year=1994|isbn=9780195146943|pages=44|oclc=27151391|quote=The nerve cell with its uninterrupted processes was described by Otto Friedrich Karl Deiters (1834-1863) in a work that was completed by Max Schultze (1825-1874) in 1865, two years after Deiters died of typhoid fever. This work portrayed the cell body with a single chief "axis cylinder" and a number of smaller "protoplasmic processes" (see figure 3.19). The latter would become known as "dendrites", a term coined by Wilhelm His (1831-1904) in 1889.}}</ref> German anatomist [[Otto Friedrich Karl Deiters]] is generally credited with the discovery of the axon by distinguishing it from the dendrites.

The term ''dendrites'' was first used in 1889 by [[Wilhelm His, Sr.|Wilhelm His]] to describe the number of smaller "protoplasmic processes" that were attached to a [[Neuron|nerve cell]].<ref>{{Cite book|title=Origins of neuroscience : a history of explorations into brain function|last=Finger|first=Stanley|publisher=Oxford University Press|year=1994|isbn=9780195146943|pages=44|oclc=27151391|quote=The nerve cell with its uninterrupted processes was described by Otto Friedrich Karl Deiters (1834-1863) in a work that was completed by Max Schultze (1825-1874) in 1865, two years after Deiters died of typhoid fever. This work portrayed the cell body with a single chief "axis cylinder" and a number of smaller "protoplasmic processes" (see figure 3.19). The latter would become known as "dendrites", a term coined by Wilhelm His (1831-1904) in 1889.}}</ref> German anatomist [[Otto Friedrich Karl Deiters]] is generally credited with the discovery of the axon by distinguishing it from the dendrites.

树突（''dendrite''）这一术语最早是在 1889 年被 [[Wilhelm His, Sr.|Wilhelm His]] 用来描述神经细胞相连的较小的“原生质突起”的数量。德国解剖学家 [[Otto Friedrich Karl Deiters]] 被认为发现了轴突，是他首先将轴突与树突区分开。

树突（''dendrite''）一词最早是在 1889 年被 [[Wilhelm His, Sr.|Wilhelm His]] 用来描述神经细胞相连的较小的“原生质突起”的数量。德国解剖学家 [[Otto Friedrich Karl Deiters]] 被认为发现了轴突，是他首先将轴突与树突区分开。

Some of the first intracellular recordings in a nervous system were made in the late 1930s by Kenneth S. Cole and Howard J. Curtis. Swiss Rüdolf Albert von Kölliker and German Robert Remak were the first to identify and characterize the axonal initial segment. Alan Hodgkin and Andrew Huxley also employed the squid giant axon (1939) and by 1952 they had obtained a full quantitative description of the ionic basis of the action potential, leading the formulation of the Hodgkin–Huxley model. Hodgkin and Huxley were awarded jointly the Nobel Prize for this work in 1963. The formulas detailing axonal conductance were extended to vertebrates in the Frankenhaeuser–Huxley equations. Louis-Antoine Ranvier was the first to describe the gaps or nodes found on axons and for this contribution these axonal features are now commonly referred to as the Nodes of Ranvier. Santiago Ramón y Cajal, a Spanish anatomist, proposed that axons were the output components of neurons. He also proposed that neurons were discrete cells that communicated with each other via specialized junctions, or spaces, between cells, now known as a synapse. Ramón y Cajal improved a silver staining process known as Golgi's method, which had been developed by his rival, Camillo Golgi.

Some of the first intracellular recordings in a nervous system were made in the late 1930s by Kenneth S. Cole and Howard J. Curtis. Swiss Rüdolf Albert von Kölliker and German Robert Remak were the first to identify and characterize the axonal initial segment. Alan Hodgkin and Andrew Huxley also employed the squid giant axon (1939) and by 1952 they had obtained a full quantitative description of the ionic basis of the action potential, leading the formulation of the Hodgkin–Huxley model. Hodgkin and Huxley were awarded jointly the Nobel Prize for this work in 1963. The formulas detailing axonal conductance were extended to vertebrates in the Frankenhaeuser–Huxley equations. Louis-Antoine Ranvier was the first to describe the gaps or nodes found on axons and for this contribution these axonal features are now commonly referred to as the Nodes of Ranvier. Santiago Ramón y Cajal, a Spanish anatomist, proposed that axons were the output components of neurons. He also proposed that neurons were discrete cells that communicated with each other via specialized junctions, or spaces, between cells, now known as a synapse. Ramón y Cajal improved a silver staining process known as Golgi's method, which had been developed by his rival, Camillo Golgi.

1930 年代末，[[Kenneth S. Cole]] 和 Howard J. Curtis 开展了最早的神经系统胞内电生理记录。瑞士人 Rüdolf Albert von Kölliker 和德国人 German Robert Remak 首先对轴突起始段进行了鉴定和性质研究。1952 年，[[Alan Hodgkin]] 和 [[Andrew Huxley]] 也使用了乌贼巨突触（1939年），到 1952 年他们得到动作电位的离子机制的完整定量描述，从而建立了 Hodgkin-Huxley 模型。Hodgkin 和 Huxley 因这项工作在 1963 年共同获得诺贝尔奖。Frankenhaeuser-Huxley 方程式则将详细描述轴突传导的公式推广到脊椎动物。Louis-Antoine Ranvier 首次描述了轴突上的不连续或饥结，因此这些轴突特征现在通常被称为郎飞结。西班牙解剖学家 Ramón y Cajal 提出轴突是神经元输出的部分<ref>{{cite journal|last=Debanne|first=D|author2=Campanac, E |author3=Bialowas, A |author4=Carlier, E |author5= Alcaraz, G |title=Axon physiology.|journal=Physiological Reviews|date=Apr 2011|volume=91|issue=2|pages=555–602|pmid=21527732 |doi=10.1152/physrev.00048.2009|url=https://hal-amu.archives-ouvertes.fr/hal-01766861/file/Debanne-Physiol-Rev-2011.pdf}}</ref>。他还提出，神经元是离散的细胞，通过细胞间的特殊连接或空隙彼此沟通，今天称为突触的结构进行相互通信。Ramón y Cajal 改进了他的竞争对手 [[Camillo Golgi]] 发明的高尔基染色法<ref>{{cite journal|last=López-Muñoz|first=F|title=Neuron theory, the cornerstone of neuroscience, on the centenary of the Nobel Prize award to Santiago Ramón y Cajal|journal=Brain Research Bulletin|volume=70|issue=4–6|pages=391–405|pmid=17027775|doi=10.1016/j.brainresbull.2006.07.010|date=October 2006|s2cid=11273256}}</ref>。

1930 年代末，[[Kenneth S. Cole]] 和 Howard J. Curtis 最先开始对神经系统进行胞内电生理记录。瑞士人 Rüdolf Albert von Kölliker 和德国人 German Robert Remak 首先对轴突起始段进行了鉴定和性质研究。1952 年，[[Alan Hodgkin]] 和 [[Andrew Huxley]] 也使用了乌贼巨突触（1939年），到 1952 年他们得到动作电位的离子机制的完整定量描述，从而建立了 Hodgkin-Huxley 模型。Hodgkin 和 Huxley 因这项工作在 1963 年共同获得诺贝尔奖。Frankenhaeuser-Huxley 方程式则将将刻画轴突传导的公式推广到脊椎动物。Louis-Antoine Ranvier 首次描述了轴突上的不连续或结，因此这些轴突特征现在通常被称为郎飞结。西班牙解剖学家 Ramón y Cajal 提出轴突是神经元输出的部分<ref>{{cite journal|last=Debanne|first=D|author2=Campanac, E |author3=Bialowas, A |author4=Carlier, E |author5= Alcaraz, G |title=Axon physiology.|journal=Physiological Reviews|date=Apr 2011|volume=91|issue=2|pages=555–602|pmid=21527732 |doi=10.1152/physrev.00048.2009|url=https://hal-amu.archives-ouvertes.fr/hal-01766861/file/Debanne-Physiol-Rev-2011.pdf}}</ref>。他还指出，神经元是离散的细胞，通过细胞间的特殊连接或空隙，即今天称为突触的结构进行相互通信。Ramón y Cajal 改进了他的竞争对手 [[Camillo Golgi]] 发明的高尔基染色法<ref>{{cite journal|last=López-Muñoz|first=F|title=Neuron theory, the cornerstone of neuroscience, on the centenary of the Nobel Prize award to Santiago Ramón y Cajal|journal=Brain Research Bulletin|volume=70|issue=4–6|pages=391–405|pmid=17027775|doi=10.1016/j.brainresbull.2006.07.010|date=October 2006|s2cid=11273256}}</ref>。

==Dendrite development 树突发育==

==Dendrite development 树突发育==

During the development of dendrites, several factors can influence differentiation. These include modulation of sensory input, environmental pollutants, body temperature, and drug use.<ref name=":0">{{cite journal|last=McEwen|first=Bruce S.|title=Stress, sex, and neural adaptation to a changing environment: mechanisms of neuronal remodeling|journal=Annals of the New York Academy of Sciences|volume=1204|pages=38–59|doi=10.1111/j.1749-6632.2010.05568.x|year=2010|bibcode=2010NYASA1204...38M|pmid=20840167|pmc=2946089}}</ref> For example, rats raised in dark environments were found to have a reduced number of spines in pyramidal cells located in the primary visual cortex and a marked change in distribution of dendrite branching in layer 4 stellate cells.<ref name=":1">{{cite journal|last=Borges|first=S.|author2=Berry, M.|title=The effects of dark rearing on the development of the visual cortex of the rat|journal=The Journal of Comparative Neurology|date=15 July 1978|volume=180|issue=2|pages=277–300|doi=10.1002/cne.901800207|pmid=659662|s2cid=42749947}}</ref> Experiments done in vitro and in vivo have shown that the presence of afferents and input activity per se can modulate the patterns in which dendrites differentiate.<ref name=Tavosanis />

During the development of dendrites, several factors can influence differentiation. These include modulation of sensory input, environmental pollutants, body temperature, and drug use.<ref name=":0">{{cite journal|last=McEwen|first=Bruce S.|title=Stress, sex, and neural adaptation to a changing environment: mechanisms of neuronal remodeling|journal=Annals of the New York Academy of Sciences|volume=1204|pages=38–59|doi=10.1111/j.1749-6632.2010.05568.x|year=2010|bibcode=2010NYASA1204...38M|pmid=20840167|pmc=2946089}}</ref> For example, rats raised in dark environments were found to have a reduced number of spines in pyramidal cells located in the primary visual cortex and a marked change in distribution of dendrite branching in layer 4 stellate cells.<ref name=":1">{{cite journal|last=Borges|first=S.|author2=Berry, M.|title=The effects of dark rearing on the development of the visual cortex of the rat|journal=The Journal of Comparative Neurology|date=15 July 1978|volume=180|issue=2|pages=277–300|doi=10.1002/cne.901800207|pmid=659662|s2cid=42749947}}</ref> Experiments done in vitro and in vivo have shown that the presence of afferents and input activity per se can modulate the patterns in which dendrites differentiate.<ref name=Tavosanis />

在树突的发育过程中，有几个因素可以影响这种分化，包括感觉输入调控、环境污染物、体温和药物使用<ref name=":0" /> 。例如，在黑暗环境中长大的大鼠，初级视皮层的锥体细胞的树突棘数量减少，在第 4 层星状细胞中树突分支的分布有明显的不同<ref name=":1" /> 。体外和体内实验表明，传入神经和传入神经活动本身可以调节树突分化的模式<ref name="Tavosanis" />。

在树突的发育过程中，有几个因素可以影响这种分化，包括感觉输入调控、环境污染物、体温和药物使用<ref name=":0" /> 。例如，在黑暗环境中长大的大鼠，初级视皮层的锥体细胞的树突棘数量减少，在第 4 层星形细胞中树突分支的分布有明显的不同<ref name=":1" /> 。体外和体内实验表明，传入神经和传入神经活动本身可以调节树突分化的模式<ref name="Tavosanis" />。

Little is known about the process by which dendrites orient themselves in vivo and are compelled to create the intricate branching pattern unique to each specific neuronal class. One theory on the mechanism of dendritic arbor development is the Synaptotropic Hypothesis. The synaptotropic hypothesis proposes that input from a presynaptic to a postsynaptic cell (and maturation of excitatory synaptic inputs) eventually can change the course of synapse formation at dendritic and axonal arbors.<ref name=":2">{{cite journal|last=Cline|first=H|author2=Haas, K|title=The regulation of dendritic arbor development and plasticity by glutamatergic synaptic input: a review of the synaptotrophic hypothesis.|journal=The Journal of Physiology|date=Mar 15, 2008|volume=586|issue=6|pages=1509–17|pmid=18202093|doi=10.1113/jphysiol.2007.150029|pmc=2375708}}</ref> This synapse formation is required for the development of neuronal structure in the functioning brain. A balance between metabolic costs of dendritic elaboration and the need to cover receptive field presumably determine the size and shape of dendrites. A complex array of extracellular and intracellular cues modulates dendrite development including transcription factors, receptor-ligand interactions, various signaling pathways, local translational machinery, cytoskeletal elements, Golgi outposts and endosomes. These contribute to the organization of the dendrites on individual cell bodies and the placement of these dendrites in the neuronal circuitry. For example, it was shown that β-actin zipcode binding protein 1 (ZBP1) contributes to proper dendritic branching. Other important transcription factors involved in the morphology of dendrites include CUT, Abrupt, Collier, Spineless, ACJ6/drifter, CREST, NEUROD1, CREB, NEUROG2 etc. Secreted proteins and cell surface receptors includes neurotrophins and tyrosine kinase receptors, BMP7, Wnt/dishevelled, EPHB 1–3, Semaphorin/plexin-neuropilin, slit-robo, netrin-frazzled, reelin. Rac, CDC42 and RhoA serve as cytoskeletal regulators and the motor protein includes KIF5, dynein, LIS1. Important secretory and endocytic pathways controlling the dendritic development include DAR3 /SAR1, DAR2/Sec23, DAR6/Rab1 etc. All these molecules interplay with each other in controlling dendritic morphogenesis including the acquisition of type specific dendritic arborization, the regulation of dendrite size and the organization of dendrites emanating from different neurons.<ref name="urbanska" /><ref name="perycz" />

Little is known about the process by which dendrites orient themselves in vivo and are compelled to create the intricate branching pattern unique to each specific neuronal class. One theory on the mechanism of dendritic arbor development is the Synaptotropic Hypothesis. The synaptotropic hypothesis proposes that input from a presynaptic to a postsynaptic cell (and maturation of excitatory synaptic inputs) eventually can change the course of synapse formation at dendritic and axonal arbors.<ref name=":2">{{cite journal|last=Cline|first=H|author2=Haas, K|title=The regulation of dendritic arbor development and plasticity by glutamatergic synaptic input: a review of the synaptotrophic hypothesis.|journal=The Journal of Physiology|date=Mar 15, 2008|volume=586|issue=6|pages=1509–17|pmid=18202093|doi=10.1113/jphysiol.2007.150029|pmc=2375708}}</ref> This synapse formation is required for the development of neuronal structure in the functioning brain. A balance between metabolic costs of dendritic elaboration and the need to cover receptive field presumably determine the size and shape of dendrites. A complex array of extracellular and intracellular cues modulates dendrite development including transcription factors, receptor-ligand interactions, various signaling pathways, local translational machinery, cytoskeletal elements, Golgi outposts and endosomes. These contribute to the organization of the dendrites on individual cell bodies and the placement of these dendrites in the neuronal circuitry. For example, it was shown that β-actin zipcode binding protein 1 (ZBP1) contributes to proper dendritic branching. Other important transcription factors involved in the morphology of dendrites include CUT, Abrupt, Collier, Spineless, ACJ6/drifter, CREST, NEUROD1, CREB, NEUROG2 etc. Secreted proteins and cell surface receptors includes neurotrophins and tyrosine kinase receptors, BMP7, Wnt/dishevelled, EPHB 1–3, Semaphorin/plexin-neuropilin, slit-robo, netrin-frazzled, reelin. Rac, CDC42 and RhoA serve as cytoskeletal regulators and the motor protein includes KIF5, dynein, LIS1. Important secretory and endocytic pathways controlling the dendritic development include DAR3 /SAR1, DAR2/Sec23, DAR6/Rab1 etc. All these molecules interplay with each other in controlling dendritic morphogenesis including the acquisition of type specific dendritic arborization, the regulation of dendrite size and the organization of dendrites emanating from different neurons.<ref name="urbanska" /><ref name="perycz" />

树突如何在体内定向，并产生特定神经元类别特有的复杂分支模式，这个过程我们知之甚少。树突分支发育机制的一个理论是突触营养假设。突触营养假设认为，突触前细胞向突触后细胞的输入（以及兴奋性突触输入的成熟）最终可以改变树突和轴突末梢的分支形成突触的进程<ref name=":2" /> 。这种突触形成对工作中的大脑的神经元结构发育所必需的。树突复杂分支的形成的代谢成本和覆盖感受野的需要之间的平衡大体决定了树突的大小和形状。一系列复杂的胞外和胞内信号，包括转录因子、受体-配体相互作用、各种信号通路、局部翻译机制、细胞骨架元件、高尔基前哨和内涵体，都会调节树突发育。这些促进了单个细胞胞体上树突的组织以及这些树突在神经回路中的定位。例如，研究表明 β 肌动蛋白结合蛋白1（β-actin zipcode binding protein 1，ZBP1）在树突形成正常分支中有作用。其他与树突形态有关的重要转录因子包括 CUT、stump、Collier、Spineless、ACJ6/drifter、CREST、NEUROD1、CREB、neurog2 等。分泌蛋白和细胞表面受体包括神经营养因子和酪氨酸受体激酶、BMP7、Wnt/dishevelled、EPHB 1-3、 Semaphorin/plexin-neuropilin、slit-robo、netrin-frazzled、reelin。Rac, CDC42 和 RhoA 作为细胞骨架调节分子，马达蛋白包括 KIF5、dynein、LIS1。控制树突发育的重要分泌和内吞途径包括 DAR3/SAR1、DAR2/Sec23、DAR6/rab1 等。所有这些分子在控制树突形态发生中相互作用，包括细胞类型特异的树突分支、树突大小和不同神经元树突的组织<ref name=urbanska /><ref name=perycz />。

树突如何在体内定向，并产生特定神经元类别特有的复杂分支模式，我们对这个过程仍知之甚少。树突分支发育机制的一个理论是突触营养假设。突触营养假设认为，突触前细胞向突触后细胞的输入（以及兴奋性突触输入的成熟）最终可以改变树突和轴突末梢的分支形成突触的进程<ref name=":2" /> 。这种突触形成对工作中的大脑的神经元结构发育是所必需的。树突复杂分支的形成的代谢成本和覆盖感受野的需要之间的平衡大体决定了树突的大小和形状。一系列复杂的胞外和胞内信号，包括转录因子、配体受体相互作用、各种信号通路、局部翻译机制、细胞骨架元件、高尔基前哨和核内体，都会调节树突发育。这些促进了单个细胞胞体上树突的组织以及这些树突在神经回路中的定位。例如，研究表明 β 肌动蛋白结合蛋白1（β-actin zipcode binding protein 1，ZBP1）在树突形成正常分支中发挥作用。其它与树突形态有关的重要转录因子包括 CUT、stump、Collier、Spineless、ACJ6/drifter、CREST、NEUROD1、CREB、neurog2 等。分泌蛋白和细胞表面受体包括神经营养因子和酪氨酸受体激酶、BMP7、Wnt/dishevelled、EPHB 1-3、 Semaphorin/plexin-neuropilin、slit-robo、netrin-frazzled、reelin。Rac, CDC42 和 RhoA 作为细胞骨架调节分子，马达蛋白包括 KIF5、dynein、LIS1。控制树突发育的重要分泌和内吞途径包括 DAR3/SAR1、DAR2/Sec23、DAR6/rab1 等。所有这些分子在控制树突形态发生，包括细胞类型特异的树突分支、树突大小和不同神经元树突的组织中相互作用<ref name=urbanska /><ref name=perycz />。

==Electrical properties 电性质==

==Electrical properties 电性质==

Dendrites were once thought to merely convey electrical stimulation passively. This passive transmission means that [[voltage]] changes measured at the cell body are the result of activation of distal synapses propagating the electric signal towards the cell body without the aid of [[voltage-gated ion channels]]. [[Cable theory|Passive cable theory]] describes how voltage changes at a particular location on a dendrite transmit this electrical signal through a system of converging dendrite segments of different diameters, lengths, and electrical properties. Based on passive cable theory one can track how changes in a neuron's dendritic morphology impacts the membrane voltage at the cell body, and thus how variation in dendrite architectures affects the overall output characteristics of the neuron.<ref name="Koch 1999">{{cite book|last=Koch|first=Christof|title=Biophysics of computation : information processing in single neurons|date=1999|publisher=Oxford Univ. Press|location=New York [u.a.]|isbn=0-19-510491-9}}</ref><ref name="Häusser 2008">{{cite book|last=Häusser|first=Michael|title=Dendrites|date=2008|publisher=Oxford University Press|location=Oxford|isbn=978-0-19-856656-4|edition=2nd}}</ref>

Dendrites were once thought to merely convey electrical stimulation passively. This passive transmission means that [[voltage]] changes measured at the cell body are the result of activation of distal synapses propagating the electric signal towards the cell body without the aid of [[voltage-gated ion channels]]. [[Cable theory|Passive cable theory]] describes how voltage changes at a particular location on a dendrite transmit this electrical signal through a system of converging dendrite segments of different diameters, lengths, and electrical properties. Based on passive cable theory one can track how changes in a neuron's dendritic morphology impacts the membrane voltage at the cell body, and thus how variation in dendrite architectures affects the overall output characteristics of the neuron.<ref name="Koch 1999">{{cite book|last=Koch|first=Christof|title=Biophysics of computation : information processing in single neurons|date=1999|publisher=Oxford Univ. Press|location=New York [u.a.]|isbn=0-19-510491-9}}</ref><ref name="Häusser 2008">{{cite book|last=Häusser|first=Michael|title=Dendrites|date=2008|publisher=Oxford University Press|location=Oxford|isbn=978-0-19-856656-4|edition=2nd}}</ref>

树突之前被认为只是被动地传导电刺激。这种被动传输意味着，在细胞体上测量到的电压变化是远端突触激活产生的电信号，在没有电压门控离子通道的帮助下，向胞体传播的结果。无源电缆理论描述了树突特定位置的电压变化如何通过不同直径、长度和电性质的汇聚的树突系统传输这种电信号。基于被动电缆理论，人们可以探究神经元树突形态的变化如何影响胞体的膜电位，从而了解树突的结构体系变化如何影响神经元的整体输出特性<ref name="Koch 1999" /><ref name="Häusser 2008" />。

之前认为树突只是被动地传导电刺激。这种被动传输意味着，在细胞体上测量到的电压变化是远端突触激活产生的电信号，在没有电压门控离子通道的帮助下，向胞体传播的结果。被动电缆理论描述了树突特定位置的电压变化如何通过向胞体汇聚的不同直径、长度和电性质的树突段组成的系统传输这种电信号。基于被动电缆理论，人们可以探究神经元树突形态的变化如何影响胞体的膜电位，从而了解树突的结构体系变化如何影响神经元的整体输出特性<ref name="Koch 1999" /><ref name="Häusser 2008" />。

Electrochemical signals are propagated by action potentials that utilize intermembrane voltage-gated ion channels to transport sodium ions, calcium ions, and potassium ions. Each ion species has its own corresponding protein channel located in the lipid bilayer of the cell membrane. The cell membrane of neurons covers the axons, cell body, dendrites, etc. The protein channels can differ between chemical species in the amount of required activation voltage and the activation duration.<ref name="Alberts 2009"/>

Electrochemical signals are propagated by action potentials that utilize intermembrane voltage-gated ion channels to transport sodium ions, calcium ions, and potassium ions. Each ion species has its own corresponding protein channel located in the lipid bilayer of the cell membrane. The cell membrane of neurons covers the axons, cell body, dendrites, etc. The protein channels can differ between chemical species in the amount of required activation voltage and the activation duration.<ref name="Alberts 2009"/>

电化学信号可以利用动作电位进行传播，动作电位使用电压门控离子通道跨膜转运钠离子、钙离子和钾离子。每种离子在细胞膜的脂质双分子层中都有自己对应的蛋白通道。神经元的细胞膜覆盖轴突、胞体、树突等。不同离子的蛋白质通道具有不同的激活电位和持续时间<ref name="Alberts 2009" />。

电化学信号可以利用动作电位进行传播，动作电位使用电压门控离子通道跨膜转运钠离子、钙离子和钾离子。每种离子在细胞膜的脂质双分子层中都有其对应的蛋白通道。神经元的细胞膜覆盖轴突、胞体、树突等。不同离子的蛋白质通道具有不同的激活电位和持续时间<ref name="Alberts 2009" />。

Action potentials in animal cells are generated by either sodium-gated or calcium-gated ion channels in the plasma membrane. These channels are closed when the membrane potential is near to, or at, the resting potential of the cell. The channels will start to open if the membrane potential increases, allowing sodium or calcium ions to flow into the cell. As more ions enter the cell, the membrane potential continues to rise. The process continues until all of the ion channels are open, causing a rapid increase in the membrane potential that then triggers the decrease in the membrane potential. The depolarizing is caused by the closing of the ion channels that prevent sodium ions from entering the neuron, and they are then actively transported out of the cell. Potassium channels are then activated, and there is an outward flow of potassium ions, returning the electrochemical gradient to the resting potential. After an action potential has occurred, there is a transient negative shift, called the afterhyperpolarization or refractory period, due to additional potassium currents. This is the mechanism that prevents an action potential from traveling back the way it just came.<ref name="Alberts 2009" /><ref name=":4">{{cite journal|last=Barnett|first=MW|author2=Larkman, PM|title=The action potential.|journal=Practical Neurology|date=Jun 2007|volume=7|issue=3|pages=192–7|pmid=17515599}}</ref>

Action potentials in animal cells are generated by either sodium-gated or calcium-gated ion channels in the plasma membrane. These channels are closed when the membrane potential is near to, or at, the resting potential of the cell. The channels will start to open if the membrane potential increases, allowing sodium or calcium ions to flow into the cell. As more ions enter the cell, the membrane potential continues to rise. The process continues until all of the ion channels are open, causing a rapid increase in the membrane potential that then triggers the decrease in the membrane potential. The depolarizing is caused by the closing of the ion channels that prevent sodium ions from entering the neuron, and they are then actively transported out of the cell. Potassium channels are then activated, and there is an outward flow of potassium ions, returning the electrochemical gradient to the resting potential. After an action potential has occurred, there is a transient negative shift, called the afterhyperpolarization or refractory period, due to additional potassium currents. This is the mechanism that prevents an action potential from traveling back the way it just came.<ref name="Alberts 2009" /><ref name=":4">{{cite journal|last=Barnett|first=MW|author2=Larkman, PM|title=The action potential.|journal=Practical Neurology|date=Jun 2007|volume=7|issue=3|pages=192–7|pmid=17515599}}</ref>

动物细胞的动作电位是由质膜上的钠门控或钙门控的离子通道产生的。这些通道在膜电位接近细胞的静息电位时关闭。随着膜电位增加，通道将开始开放，使钠离子或钙离子流入细胞。随着更多的离子进入细胞，膜电位会继续上升。这个过程一直持续到所有的离子通道都打开，导致膜电位的快速增加，然后触发膜电位的减少。去极化是因为钠离子打开，然后钠离子外流。然后激活钾离子通道，钾离子外流，将电化学梯度回到静息电位。动作电位发生后，由于额外的钾电流，膜电位会有一个短暂的负移，称为后超极化或不应期。这种机制可以阻止动作电位逆向传播<ref name="Alberts 2009"/><ref name=":4" />。

动物细胞的动作电位是由质膜上的钠门控或钙门控的离子通道产生的。这些通道在膜电位接近细胞的静息电位时是关闭的。随着膜电位增加，通道将开始打开，使钠离子或钙离子流入细胞。随着更多的离子进入细胞，膜电位会继续上升。这个过程一直持续到所有的离子通道都打开，导致膜电位的快速增加，然后触发膜电位的减少。去极化是因为钠离子打开，然后钠离子外流。然后激活钾离子通道，钾离子外流，将电化学梯度带回到静息电位。动作电位发生后，由于额外的钾电流，膜电位会有一个短暂的负移，称为后超极化或不应期。这种机制可以阻止动作电位逆向传播<ref name="Alberts 2009"/><ref name=":4" />。

Another important feature of dendrites, endowed by their active voltage gated conductance, is their ability to send action potentials back into the dendritic arbor. Known as [[Neural backpropagation|back-propagating]] action potentials, these signals depolarize the dendritic arbor and provide a crucial component toward synapse modulation and [[long-term potentiation]]. Furthermore, a train of back-propagating action potentials artificially generated at the soma can induce a calcium action potential (a [[dendritic spike]]) at the dendritic initiation zone in certain types of neurons.{{citation needed|date=June 2015}}

Another important feature of dendrites, endowed by their active voltage gated conductance, is their ability to send action potentials back into the dendritic arbor. Known as [[Neural backpropagation|back-propagating]] action potentials, these signals depolarize the dendritic arbor and provide a crucial component toward synapse modulation and [[long-term potentiation]]. Furthermore, a train of back-propagating action potentials artificially generated at the soma can induce a calcium action potential (a [[dendritic spike]]) at the dendritic initiation zone in certain types of neurons.{{citation needed|date=June 2015}}

==Plasticity 可塑性==

==Plasticity 可塑性==

Dendrites themselves appear to be capable of [[synaptic plasticity|plastic changes]] during the adult life of animals, including invertebrates. Neuronal dendrites have various compartments known as functional units that are able to compute incoming stimuli. These functional units are involved in processing input and are composed of the subdomains of dendrites such as spines, branches, or groupings of branches. Therefore, plasticity that leads to changes in the dendrite structure will affect communication and processing in the cell. During development, dendrite morphology is shaped by intrinsic programs within the cell's genome and extrinsic factors such as signals from other cells. But in adult life, extrinsic signals become more influential and cause more significant changes in dendrite structure compared to intrinsic signals during development. In females, the dendritic structure can change as a result of physiological conditions induced by hormones during periods such as pregnancy, lactation, and following the estrous cycle. This is particularly visible in pyramidal cells of the CA1 region of the hippocampus, where the density of dendrites can vary up to 30%.<ref name=Tavosanis />

Dendrites themselves appear to be capable of [[synaptic plasticity|plastic changes]] during the adult life of animals, including invertebrates. Neuronal dendrites have various compartments known as functional units that are able to compute incoming stimuli. These functional units are involved in processing input and are composed of the subdomains of dendrites such as spines, branches, or groupings of branches. Therefore, plasticity that leads to changes in the dendrite structure will affect communication and processing in the cell. During development, dendrite morphology is shaped by intrinsic programs within the cell's genome and extrinsic factors such as signals from other cells. But in adult life, extrinsic signals become more influential and cause more significant changes in dendrite structure compared to intrinsic signals during development. In females, the dendritic structure can change as a result of physiological conditions induced by hormones during periods such as pregnancy, lactation, and following the estrous cycle. This is particularly visible in pyramidal cells of the CA1 region of the hippocampus, where the density of dendrites can vary up to 30%.<ref name=Tavosanis />

树突在动物包括无脊椎动物的成年生命阶段似乎能够发生可塑性变化。神经元树突有许多被称为功能单元的区域，它们能够对传入的刺激进行计算。这些功能单元参与处理的输入，由树突的子域，如树突棘、分支或分支组组成。因此，引起树突结构变化的可塑性将影响细胞的通信和处理。在发育过程中，树突形态是由细胞基因组编码的内在程序和（来自其他细胞的信号）外在因子塑造的。但在成年阶段，相比于发育阶段，外源信号相比于内源信号，对树突结构的影响更为显著。在女性，树突结构可以因激素诱导的生理状态如怀孕、哺乳、动情周期期间而改变。这在海马 CA1 区的锥体细胞中尤其明显，其树突密度的变化可达30% <ref name="Tavosanis" />。

树突在动物包括无脊椎动物的成年阶段似乎能够发生可塑性变化。神经元树突有称为功能单元的各种分区，它们能够对传入的刺激进行计算。这些功能单元由树突棘、分支或分支组等树突子结构组成，对输入进行处理。因此，导致树突结构变化的可塑性将影响细胞的通信和处理。在发育过程中，树突形态是由细胞基因组编码的内在程序和来自其他细胞的信号等外部因子塑造的。但在成年阶段，相比于发育阶段，外部信号相比于内源信号，对树突结构的影响更为显著。女性在怀孕、哺乳、动情周期等激素诱导的生理状态会引起树突结构的变化。这在海马 CA1 区的锥体细胞中尤其明显，其树突密度的变化可达 30% <ref name="Tavosanis" />。

==Notes==

==Notes==