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在神经系统中，神经元（即神经细胞）通过称为'''突触'''<ref name=":0">{{cite book|last1=Foster|first1=M.|last2=Sherrington|first2=C.S.|title=Textbook of Physiology, volume 3|date=1897|publisher=Macmillan|location=London|page=929|edition=7th}}</ref> 的结构，将电信号或化学信号传递给其他神经元或效应靶细胞。
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{{Short description|Structure of neurons in the nervous system}}
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突触对于神经冲动在神经元之间传递是至关重要的。神经元是特化的向靶细胞传递信号的细胞，突触正是它们传递信号的手段。在突触处，传递信号的神经元（突触前神经元）与目标细胞(突触后细胞)的质膜紧密相对。突触前和突触后位点都包含大量的分子结构阵列，这些分子结构连接两个膜并执行信号传导过程<ref name=":2">{{cite journal |last1=Perea |first1=G. |last2=Navarrete |first2=M. |last3=Araque |first3=A. |date=August 2009 |title=Tripartite synapses: astrocytes process and control synaptic information |journal=[[Trends (journals)|Trends in Neurosciences]] |volume=32 |issue=8 |pages=421–431 |location=Cambridge, MA |publisher=[[Cell Press]] |pmid=19615761 |doi=10.1016/j.tins.2009.05.001 |s2cid=16355401 }}</ref> 。在许多突触中，突触前部分位于轴突，突触后部分位于树突或胞体上。星形胶质细胞也与突触神经元交换信息，对突触活动做出反应，从而调节神经传导。突触前和突触后神经元的突触粘附分子（SAMs）部分重叠而粘附在一起，将突触（至少化学突触）稳定在其位置；SAMs 也可能有助于突触的产生与功能<ref name=":3">{{cite journal | pmc = 3312681 | pmid=22278667 | doi=10.1101/cshperspect.a005694 | volume=4 | issue=4 | title=Synaptic cell adhesion | year=2012 | journal=Cold Spring Harb Perspect Biol | pages=a005694 | last1 = Missler | first1 = M | last2 = Südhof | first2 = TC | last3 = Biederer | first3 = T}}</ref>。
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{{About|synapses of the nervous system||3=Synapse (disambiguation)}}
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{{Synapse map}}
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{{Presynaptic_synapse}}
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一些作者将突触的概念进行了扩展，以包括从神经元到任何其他细胞类型，比如到运动细胞（尽管这种非神经元的接触可能被称为接头，一个有些历史的术语）的通讯<ref name=":4">{{cite book |last1=Schacter |first1=Daniel L. |author-link1=Daniel Schacter |last2=Gilbert |first2=Daniel T. |author-link2=Daniel Gilbert (psychologist) |last3=Wegner |first3=Daniel M. |author-link3=Daniel Wegner |title=Psychology |url=https://archive.org/details/psychology0000scha |url-access=registration |edition=2nd |year=2011 |publisher=Worth Publishers |location=New York |page=[https://archive.org/details/psychology0000scha/page/80 80] |isbn=978-1-4292-3719-2 |oclc=696604625 |lccn=2010940234}}</ref> 。Sanford Palay 的一项具有里程碑意义的研究证明了突触的存在<ref name=":5">{{Cite journal|last=Palay|first=Sanford|title=Synapses in the central nervous system|journal=J Biophys Biochem Cytol|volume=2|issue=4|pages=193–202|doi=10.1083/jcb.2.4.193|pmc=2229686|pmid=13357542|year=1956}}</ref>。
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In the [[nervous system]], a '''synapse'''<ref name=":0">{{cite book|last1=Foster|first1=M.|last2=Sherrington|first2=C.S.|title=Textbook of Physiology, volume 3|date=1897|publisher=Macmillan|location=London|page=929|edition=7th}}</ref> is a structure that permits a [[neuron]] (or nerve cell) to pass an electrical or chemical signal to another neuron or to the target effector cell.
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==概念的历史==
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[[Santiago Ramón y Cajal]] 提出身体内的神经元之间并不是连续的，但仍然相互交流，即所谓的神经元学说<ref name=":6">{{cite book |last1=Elias |first1=Lorin J. |last2=Saucier |first2=Deborah M. |title=Neuropsychology: Clinical and Experimental Foundations |year=2006 |publisher=[[Pearson Education|Pearson/Allyn & Bacon]] |location=Boston |isbn=978-0-20534361-4 |oclc=61131869 |lccn=2005051341}}</ref> 。突触的英文单词（synapse）是由英国神经生理学家 [[Charles Scott Sherrington|Charles Sherrington]] 于1897年在迈克尔 · 福斯特的《生理学教科书》中引入的 <ref name=":0" /> 。Sherrington 想找个好用的名词，以突出两个独立单元之间的结合，而实际上“synapse”一词是由福斯特的朋友、英国古典学者 [[Arthur Woollgar Verrall]] 提议的 <ref name=":7">{{cite web|title=synapse|url=http://www.etymonline.com/index.php?term=synapse|publisher=[[Online Etymology Dictionary]]|access-date=2013-10-01|url-status=live|archive-url=https://web.archive.org/web/20131214051016/http://www.etymonline.com/index.php?term=synapse|archive-date=2013-12-14}}</ref><ref name=":8">{{cite journal |last=Tansey |first=E.M. |year=1997 |title=Not committing barbarisms: Sherrington and the synapse, 1897 |journal=[[Brain Research Bulletin]] |volume=44 |issue=3 |pages=211–212 |location=Amsterdam |publisher=[[Elsevier]] |pmid=9323432 |doi=10.1016/S0361-9230(97)00312-2 |s2cid=40333336 |quote=The word synapse first appeared in 1897, in the seventh edition of Michael Foster's ''Textbook of Physiology''.}}</ref> 。这个词来源于希腊语 synapsis，意指“连接”，它又来源于“together”和“ to fasten”。
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在神经系统中，神经元（即神经细胞）通过称为突触<ref name=":0" /> 的结构，将电信号或化学信号传递给其他神经元或效应靶细胞。
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突触间隙当时作为理论上的构造，有被表述为轴突末端与树突或胞体之间的不连续性。但这种突触前后膜的分离，现在我们知道约有 20 纳米，用当时最好的光学显微镜进行组织学观察是无法分辨的。直到 20 世纪 50 年代，用电子显微镜才显示了突触的精细结构，突触前和突触后分离的、平行的细胞膜与突起，以及两者之间的间隙<ref name=":9">{{cite journal|last1=De Robertis|first=Eduardo D.P.|last2=Bennett|first2=H. Stanley|title=Some features of the submicroscopic morphology of synapses in frog and earthworm|journal=Journal of Biophysical and Biochemical Cytology|date=1955|volume=1|issue=1|pages=47-58|doi=10.1083/jcb.1.1.47|url=https://rupress.org/jcb/article-pdf/1/1/47/1050739/47.pdf|pmc=2223594}}</ref><ref name=":10">{{cite journal|last1=Palay|first1=Sanford L.|last2=Palade|first2=George E.|title=The fine structure of neurons|journal=Journal of Biophysical and Biochemical Cytology|date=1955|volume=1|issue=1|pages=69-88|doi=10.1083/jcb.1.1.69|url=https://rupress.org/jcb/article-pdf/1/1/69/1050737/69.pdf|pmc=2223597}}</ref>。
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Synapses are essential to the transmission of nervous impulses from one neuron to another. Neurons are specialized to pass signals to individual target cells, and synapses are the means by which they do so. At a synapse, the [[plasma membrane]] of the signal-passing neuron (the ''presynaptic'' neuron) comes into close apposition with the membrane of the target (''postsynaptic'') cell.  Both the presynaptic and postsynaptic sites contain extensive arrays of [[Molecular biology|molecular machinery]] that link the two membranes together and carry out the signaling process.  In many synapses, the presynaptic part is located on an [[axon]] and the postsynaptic part is located on a [[dendrite]] or [[soma (biology)|soma]]. [[Astrocyte]]s also exchange information with the synaptic neurons, responding to synaptic activity and, in turn, regulating [[neurotransmission]].<ref name=":2">{{cite journal |last1=Perea |first1=G. |last2=Navarrete |first2=M. |last3=Araque |first3=A. |date=August 2009 |title=Tripartite synapses: astrocytes process and control synaptic information |journal=[[Trends (journals)|Trends in Neurosciences]] |volume=32 |issue=8 |pages=421–431 |location=Cambridge, MA |publisher=[[Cell Press]] |pmid=19615761 |doi=10.1016/j.tins.2009.05.001 |s2cid=16355401 }}</ref> Synapses (at least chemical synapses) are stabilized in position by synaptic adhesion molecules (SAMs) projecting from both the pre- and post-synaptic neuron and sticking together where they overlap; SAMs may also assist in the generation and functioning of synapses.<ref name=":3">{{cite journal | pmc = 3312681 | pmid=22278667 | doi=10.1101/cshperspect.a005694 | volume=4 | issue=4 | title=Synaptic cell adhesion | year=2012 | journal=Cold Spring Harb Perspect Biol | pages=a005694 | last1 = Missler | first1 = M | last2 = Südhof | first2 = TC | last3 = Biederer | first3 = T}}</ref>
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==化学突触和电突触==
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[[文件:1280px-Neuro Muscular Junction.png|链接=link=Special:FilePath/Neuro_Muscular_Junction.png|替代=|缩略图|An example of chemical synapse by the release of [[neurotransmitter]]s like [[acetylcholine]] or [[glutamic acid]].]]存在两种完全不同类型的突触：
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突触对于神经冲动在神经元之间传递是至关重要的。神经元是特化的向靶细胞传递信号的细胞，突触正是它们传递信号的手段。在突触处，传递信号的神经元（突触前神经元）与的质膜与目标细胞(突触后细胞)的质膜紧密相连。突触前和突触后位点都包含大量的分子结构阵列，这些分子结构连接两个膜并执行信号传导过程<ref name=":2" /> 。在许多突触中，突触前部分位于轴突，突触后部分位于树突或胞体上。星形胶质细胞也与突触神经元交换信息，对突触活动做出反应，从而调节神经传导。突触(至少是化学突触)通过突触前和突触后神经元发出的突触粘附分子(SAMs)并在它们重叠的地方粘附在一起而稳定在位置上; SAMs 也可能有助于突触的产生和功能<ref name=":3" />。
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* 在化学突触，突触前神经元的电活动（通过激活电压门控钙通道）被转化为称为神经递质的化学物质的释放。神经递质可与位于突触后膜上的受体结合，从而引起电反应，或通过第二信使通路激发或抑制突触后神经元。化学突触可以根据所释放的神经递质进行分类： 谷氨酸能（通常是兴奋性的)、GABA能（通常是抑制性的)、胆碱能（比如，脊椎动物神经肌肉接头）和肾上腺素能（释放去甲肾上腺素）。由于受体信号转导的复杂性，化学突触可以对突触后细胞产生复杂的效应。
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* 电突触，突触前、后的细胞膜通过特殊的称为缝隙连接的通道连接。这些通道允许电流通过，使得突触前细胞的电压变化能引起突触后细胞的电位变化。电突触的主要优点是细胞间的信号传递是极快的<ref name=":1">{{cite book |last=Silverthorn |first=Dee Unglaub |others=Illustration coordinator William C. Ober; illustrations by Claire W. Garrison; clinical consultant Andrew C. Silverthorn; contributions by Bruce R. Johnson |title=Human Physiology: An Integrated Approach |edition=4th |year=2007 |publisher=[[Pearson Education|Pearson/Benjamin Cummings]] |location=San Francisco |page=271 |isbn=978-0-8053-6851-2 |oclc=62742632 |lccn=2005056517}}</ref>。
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Some authors generalize the concept of the synapse to include the communication from a neuron to any other cell type,<ref name=":4">{{cite book |last1=Schacter |first1=Daniel L. |author-link1=Daniel Schacter |last2=Gilbert |first2=Daniel T. |author-link2=Daniel Gilbert (psychologist) |last3=Wegner |first3=Daniel M. |author-link3=Daniel Wegner |title=Psychology |url=https://archive.org/details/psychology0000scha |url-access=registration |edition=2nd |year=2011 |publisher=Worth Publishers |location=New York |page=[https://archive.org/details/psychology0000scha/page/80 80] |isbn=978-1-4292-3719-2 |oclc=696604625 |lccn=2010940234}}</ref> such as to a motor cell, although such non-neuronal contacts may be referred to as [[Neuromuscular Junction|junctions]] (a historically older term). A landmark study by [[Sanford Palay]] demonstrated the existence of synapses.<ref name=":5">{{Cite journal|last=Palay|first=Sanford|title=Synapses in the central nervous system|journal=J Biophys Biochem Cytol|volume=2|issue=4|pages=193–202|doi=10.1083/jcb.2.4.193|pmc=2229686|pmid=13357542|year=1956}}</ref>
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一些作者概括了突触的概念，包括从神经元到任何其他细胞类型的通讯<ref name=":4" /> ，比如到运动细胞，尽管这种非神经元的接触可能被称为连接(一个历史悠久的术语)。Sanford Palay 的一项具有里程碑意义的研究证明了突触的存在<ref name=":5" />。
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==History of the concept 概念史==
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[[Santiago Ramón y Cajal]] proposed that neurons are not continuous throughout the body, yet still communicate with each other, an idea known as the [[neuron doctrine]].<ref name=":6">{{cite book |last1=Elias |first1=Lorin J. |last2=Saucier |first2=Deborah M. |title=Neuropsychology: Clinical and Experimental Foundations |year=2006 |publisher=[[Pearson Education|Pearson/Allyn & Bacon]] |location=Boston |isbn=978-0-20534361-4 |oclc=61131869 |lccn=2005051341}}</ref> The word "synapse" was introduced in 1897 by the English neurophysiologist [[Charles Scott Sherrington|Charles Sherrington]] in [[Michael Foster (physiologist)|Michael Foster]]'s ''Textbook of Physiology''.<ref name=":0" /> Sherrington struggled to find a good term that emphasized a union between two ''separate'' elements, and the actual term "synapse" was suggested by the English classical scholar [[Arthur Woollgar Verrall]], a friend of Foster.<ref name=":7">{{cite web|title=synapse|url=http://www.etymonline.com/index.php?term=synapse|publisher=[[Online Etymology Dictionary]]|access-date=2013-10-01|url-status=live|archive-url=https://web.archive.org/web/20131214051016/http://www.etymonline.com/index.php?term=synapse|archive-date=2013-12-14}}</ref><ref name=":8">{{cite journal |last=Tansey |first=E.M. |year=1997 |title=Not committing barbarisms: Sherrington and the synapse, 1897 |journal=[[Brain Research Bulletin]] |volume=44 |issue=3 |pages=211–212 |location=Amsterdam |publisher=[[Elsevier]] |pmid=9323432 |doi=10.1016/S0361-9230(97)00312-2 |s2cid=40333336 |quote=The word synapse first appeared in 1897, in the seventh edition of Michael Foster's ''Textbook of Physiology''.}}</ref> The word was derived from the Greek synapsis (), meaning "conjunction", which in turn derives from  ( ("together")  and  ("to fasten"))
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这个概念的历史提出了神经元并不是连续的在整个身体里，但仍然相互交流，这个想法被称为神经元学说.<ref name=":6" /> 。圣地亚哥·拉蒙-卡哈尔。“ synapse”一词是由英国神经生理学家查尔斯 · 谢林顿于1897年在迈克尔 · 福斯特的《生理学教科书》中提出的.<ref name=":0" /> 。谢林顿努力寻找一个好的术语，强调两个独立的元素之间的结合，而实际的术语“突触”是由福斯特的朋友、英国古典学者亚瑟 · 伍尔加 · 维拉尔提出的.<ref name=":7" /><ref name=":8" /> 。这个词来源于希腊语 synapsis () ，意思是“连接”，它又来源于((“ together”)和(“ to fail”))
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However, while the synaptic gap remained a theoretical construct, and sometimes reported as a discontinuity between contiguous axonal terminations and dendrites or cell bodies, histological methods using the best light microscopes of the day could not visually resolve their separation which is now known to be about 20nm. It needed the electron microscope in the 1950s to show the finer structure of the synapse with its separate, parallel pre- and postsynaptic membranes and processes, and the cleft between the two.<ref name=":9">{{cite journal|last1=De Robertis|first=Eduardo D.P.|last2=Bennett|first2=H. Stanley|title=Some features of the submicroscopic morphology of synapses in frog and earthworm|journal=Journal of Biophysical and Biochemical Cytology|date=1955|volume=1|issue=1|pages=47-58|doi=10.1083/jcb.1.1.47|url=https://rupress.org/jcb/article-pdf/1/1/47/1050739/47.pdf|pmc=2223594}}</ref><ref name=":10">{{cite journal|last1=Palay|first1=Sanford L.|last2=Palade|first2=George E.|title=The fine structure of neurons|journal=Journal of Biophysical and Biochemical Cytology|date=1955|volume=1|issue=1|pages=69-88|doi=10.1083/jcb.1.1.69|url=https://rupress.org/jcb/article-pdf/1/1/69/1050737/69.pdf|pmc=2223597}}</ref>
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然而，虽然突触间隙仍然是一个理论上的构造，有时被报道为轴突末端与树突或细胞体之间的不连续性，但是使用当时最好的光学显微镜的组织学方法无法直观地解决它们的分离问题，现在我们知道它们大约在20纳米左右。它需要在20世纪50年代的电子显微镜显示突触的精细结构，它的独立的，平行的突触前和突触后膜和过程，以及两者之间的裂隙。.<ref name=":9" /><ref name=":10" />
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==Chemical and electrical synapses电突触和化学突触==
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[[文件:1280px-Neuro Muscular Junction.png|链接=link=Special:FilePath/Neuro_Muscular_Junction.png|替代=|缩略图|An example of chemical synapse by the release of [[neurotransmitter]]s like [[acetylcholine]] or [[glutamic acid]].]]
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There are two fundamentally different types of synapses:
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* In a [[chemical synapse]], electrical activity in the presynaptic neuron is converted (via the activation of [[Voltage-dependent calcium channel|voltage-gated calcium channels]]) into the release of a chemical called a [[neurotransmitter]] that binds to [[neurotransmitter receptor|receptors]] located in the plasma membrane of the postsynaptic cell. The neurotransmitter may initiate an electrical response or a secondary messenger pathway that may either excite or inhibit the postsynaptic neuron. Chemical synapses can be classified according to the neurotransmitter released: [[Glutamic acid|glutamatergic]] (often excitatory), [[gamma-Aminobutyric acid|GABAergic]] (often inhibitory), [[cholinergic]] (e.g. vertebrate [[neuromuscular junction]]), and [[Adrenergic receptor|adrenergic]] (releasing [[norepinephrine]]). Because of the complexity of receptor [[signal transduction]], chemical synapses can have complex effects on the postsynaptic cell.
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* In an [[electrical synapse]], the presynaptic and postsynaptic cell membranes are connected by special channels called [[gap junction]]s that are capable of passing an electric current, causing voltage changes in the presynaptic cell to induce voltage changes in the postsynaptic cell. The main advantage of an electrical synapse is the rapid transfer of signals from one cell to the next.<ref name=":1">{{cite book |last=Silverthorn |first=Dee Unglaub |others=Illustration coordinator William C. Ober; illustrations by Claire W. Garrison; clinical consultant Andrew C. Silverthorn; contributions by Bruce R. Johnson |title=Human Physiology: An Integrated Approach |edition=4th |year=2007 |publisher=[[Pearson Education|Pearson/Benjamin Cummings]] |location=San Francisco |page=271 |isbn=978-0-8053-6851-2 |oclc=62742632 |lccn=2005056517}}</ref>
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存在两种完全不同的类型的突触：
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* 在化学突触，突触前神经元的电活动（通过激活电压门控钙通道）被转化为称为神经递质的化学物质的释放。神经递质可与位于突触后细胞质膜上的受体结合，从而引起电反应，或第二信使通路激发或抑制突触后神经元。化学突触可以根据释放的神经递质进行分类： 谷氨酸能(通常是兴奋性的)、GABA能(通常是抑制性的)、胆碱能(通常是抑制性的)。脊椎动物神经肌肉接点)和肾上腺素(释放去甲肾上腺素)。由于受体信号转导的复杂性，化学突触可以对突触后细胞产生复杂的影响。
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* 电突触，突触前细胞膜和突触后细胞膜通过特殊的称为缝隙连接的通道蛋白连接。缝隙连接能够通过电流，使得突触前细胞的电压变化引起突触后细胞的电位变化。电突触的主要优点是细胞间的信号传递是极快的。<ref name=":1" />
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Synaptic communication is distinct from an [[ephaptic coupling]], in which communication between neurons occurs via indirect electric fields.
      
不同于突触通信，假突触耦合允许神经元之间通过间接的电场进行通信。
 
不同于突触通信，假突触耦合允许神经元之间通过间接的电场进行通信。
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An [[autapse]] is a chemical or electrical synapse that forms when the axon of one neuron synapses onto dendrites of the same neuron.
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自突触是一类化学突触或电突触，神经元的轴突会与自身的树突形成突触。
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自突触是一类化学突触或电突触，其轴突会与自身的树突形成突触。
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==接合类型==
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突触可以按构成突触前和突触后的神经元部位进行分类。哺乳动物神经系统中的绝大多数突触是经典的轴树突触(轴突到树突的突触) ，然而存在其它的排列方式，包括但不限于轴轴突触、树树突触、轴分泌突触、体树突触、树体突触和体体突触。
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==Types of interfaces接合类型==
  −
Synapses can be classified by the type of cellular structures serving as the pre- and post-synaptic components. The vast majority of synapses in the mammalian nervous system are classical axo-dendritic synapses (axon synapsing upon a dendrite), however, a variety of other arrangements exist. These include but are not limited to [[Axo-axonic synapse|axo-axonic]], [[Dendrodendritic synapse|dendro-dendritic]], axo-secretory, somato-dendritic, dendro-somatic, and somato-somatic synapses.
  −
 
  −
突触可以按构成突触前和突触后的细胞结构类型进行分类。哺乳动物神经系统中的绝大多数突触是典型的轴树突触(轴突到树突的突触) ，然而，还存在其他的不同排列方式。这些突触包括但不限于轴轴突触、树树突触、轴分泌突触、体树突触、树体突触和体体突触。
  −
 
  −
The axon can synapse onto a dendrite, onto a cell body, or onto another axon or axon terminal, as well as into the bloodstream or diffusely into the adjacent nervous tissue.
      
轴突跨突触释放神经递质于树突、胞体、其他轴突或轴突末梢，也可以进入血流或扩散到邻近的神经组织。
 
轴突跨突触释放神经递质于树突、胞体、其他轴突或轴突末梢，也可以进入血流或扩散到邻近的神经组织。
    
[[文件:Blausen 0843 SynapseTypes.png|链接=link=Special:FilePath/Blausen_0843_SynapseTypes.png|替代=|居中|缩略图|Different types of synapses]]
 
[[文件:Blausen 0843 SynapseTypes.png|链接=link=Special:FilePath/Blausen_0843_SynapseTypes.png|替代=|居中|缩略图|Different types of synapses]]
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thumb|500px|center|Different types of synapses
+
==记忆中的作用==
−
 
+
{{Main|Hebbian theory}}突触在记忆形成中的重要作用已获广泛的认可。当神经递质跨突触间隙后激活受体时，突触前后的两个神经元如果是同时发生活跃时，两者之间的连接就会加强，这是受体信号通路机制产生的结果。两个神经通路之间的连接强度可以存储信息，从而产生了记忆。这种突触强化的过程被称为长时程增强<ref>{{cite journal |last=Lynch |first=M. A. |date=January 1, 2004 |title=Long-Term Potentiation and Memory |journal=[[Physiological Reviews]] |volume=84 |issue=1 |pages=87–136 |pmid=14715912 |doi=10.1152/physrev.00014.2003 |url=https://zenodo.org/record/896261 }}</ref>。
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  −
拇指 | 500px | 中心 | 不同类型的突触
  −
 
  −
==Role in memory 记忆中的作用==
  −
{{Main|Hebbian theory}}
  −
It is widely accepted that the synapse plays a role in the formation of [[memory]]. As neurotransmitters activate receptors across the synaptic cleft, the connection between the two neurons is strengthened when both neurons are active at the same time, as a result of the receptor's signaling mechanisms. The strength of two connected neural pathways is thought to result in the storage of information, resulting in memory. This process of synaptic strengthening is known as [[long-term potentiation]].<ref>{{cite journal |last=Lynch |first=M. A. |date=January 1, 2004 |title=Long-Term Potentiation and Memory |journal=[[Physiological Reviews]] |volume=84 |issue=1 |pages=87–136 |pmid=14715912 |doi=10.1152/physrev.00014.2003 |url=https://zenodo.org/record/896261 }}</ref>
  −
 
  −
突触在记忆形成中起着重要作用，这是广为接受的。当神经递质跨突触间隙后激活受体时，突触前后的两个神经元如果是同时活跃时，两者之间的联系就会加强，这是受体信号通路机制的结果。两个神经通路之间的连接强度可以存储信息，从而产生了记忆。这种突触强化的过程被称为长时程增强。
  −
 
  −
By altering the release of neurotransmitters, the plasticity of synapses can be controlled in the presynaptic cell. The postsynaptic cell can be regulated by altering the function and number of its receptors. Changes in postsynaptic signaling are most commonly associated with a [[NMDA|N-methyl-d-aspartic acid]] receptor (NMDAR)-dependent long-term potentiation (LTP) and [[long-term depression]] (LTD) due to the influx of calcium into the post-synaptic cell, which are the most analyzed forms of plasticity at excitatory synapses.<ref name=":11">{{cite journal |last1=Krugers |first1=Harm J. |last2=Zhou |first2=Ming |last3=Joëls |first3= Marian |last4=Kindt |first4=Merel |date=October 11, 2011 |title=Regulation of Excitatory Synapses and Fearful Memories by Stress Hormones |journal=Frontiers in Behavioral Neuroscience |volume=5 |pages=62 |location=Switzerland |publisher=[[Frontiers (publisher)|Frontiers Media SA]] |doi=10.3389/fnbeh.2011.00062 |pmc=3190121 |pmid=22013419|doi-access=free }}</ref>
  −
 
  −
突触的可塑性可以通过改变神经递质的释放，在突触前细胞中进行控制；也可以通过改变其受体的数量和功能，在突触后细胞进行调节。突触后信号的改变，多与突触后细胞钙内流引起的N-甲基-D-天冬氨酸受体(NMDAR)依赖的长时程增强和长时程抑制有关。LTP和LTD是研究最多的兴奋性突触可塑性形式<ref name=":11" />。
  −
 
  −
==Study models 研究模型==
  −
For technical reasons, synaptic structure and function have been historically studied at unusually large [[Model organism|model]] synapses, for example:
  −
* [[Squid giant synapse]]
  −
* [[Neuromuscular junction]] (NMJ), a cholinergic synapse in vertebrates, glutamatergic in insects
  −
* Ciliary calyx in the ciliary ganglion of chicks<ref name=":12">{{cite journal|last1=Stanley|first1=EF|title=The calyx-type synapse of the chick ciliary ganglion as a model of fast cholinergic transmission.|journal=Canadian Journal of Physiology and Pharmacology|date=1992|volume=70 Suppl|pages=S73-7|pmid=1338300|doi=10.1139/y92-246}}</ref>
  −
* [[Calyx of Held]] in the brainstem
  −
* [[Ribbon synapse]] in the retina
  −
* [[Schaffer collateral]] synapse in the [[hippocampus]]
  −
 
  −
由于技术原因，历史上对突触结构和功能的研究都是在大型突触模型上进行的，例如:
  −
* 乌贼巨大突触
  −
* 神经肌肉接点，脊椎动物的胆碱能突触，昆虫的谷氨酸能突触，
  −
* 小鸡睫状神经节的睫状体花萼，Ciliary calyx in the ciliary ganglion of chicks<ref name=":12" />
  −
* 视网膜的掌侧突触，
  −
* 海马的 Schaffer 突触
  −
 
  −
==Synaptic polarization 突触极性==
  −
The function of neurons depends upon [[cell polarity]]. The distinctive structure of nerve cells allows [[action potential]]s to travel directionally (from dendrites to cell body down the axon), and for these signals to then be received and carried on by post-synaptic neurons or received by effector cells. Nerve cells have long been used as models for cellular polarization, and of particular interest are the mechanisms underlying the polarized localization of synaptic molecules. [[Phosphatidylinositol 4,5-bisphosphate|PIP2]] signaling regulated by [[Inositol monophosphatase|IMPase]] plays an integral role in synaptic polarity.
     −
= = 突触极化 = = 神经元的功能取决于细胞极性。神经细胞独特的结构使得动作电位可以定向传递(从树突到细胞体再到轴突) ，这些信号可以被突触后神经元接收和传递，或者被效应细胞接收。长期以来，神经细胞一直被用作细胞极化的模型，特别感兴趣的是极化定位突触分子的机制。Pip2信号通路受 IMPase 调节，在突触极性中起着重要作用。
+
突触的可塑性可以通过改变神经递质释放，从而在突触前细胞中进行控制；也可以通过改变细胞膜上受体的数量和功能，在突触后细胞进行调节。突触后信号的改变，多与突触后细胞钙内流引起的 N-甲基-D-天冬氨酸受体（NMDAR）依赖的长时程增强（long-term potentiation, LTP）和长时程抑制（[[long-term depression|long-term depression,]] LTD）有关。LTP 和 LTD 是研究最多的兴奋性突触可塑性形式<ref name=":11">{{cite journal |last1=Krugers |first1=Harm J. |last2=Zhou |first2=Ming |last3=Joëls |first3= Marian |last4=Kindt |first4=Merel |date=October 11, 2011 |title=Regulation of Excitatory Synapses and Fearful Memories by Stress Hormones |journal=Frontiers in Behavioral Neuroscience |volume=5 |pages=62 |location=Switzerland |publisher=[[Frontiers (publisher)|Frontiers Media SA]] |doi=10.3389/fnbeh.2011.00062 |pmc=3190121 |pmid=22013419|doi-access=free }}</ref>。
    +
==研究模型==
 +
因技术原因，历史上对突触结构和功能的研究都是在较大的突触模型上进行的，例如:
 +
* 乌贼的巨突触
 +
* 神经肌肉接头，在脊椎动物是胆碱能，昆虫中是谷氨酸能
 +
* 鸡的睫状神经节的睫状体萼<ref name=":12">{{cite journal|last1=Stanley|first1=EF|title=The calyx-type synapse of the chick ciliary ganglion as a model of fast cholinergic transmission.|journal=Canadian Journal of Physiology and Pharmacology|date=1992|volume=70 Suppl|pages=S73-7|pmid=1338300|doi=10.1139/y92-246}}</ref>
 +
* 视网膜的带突触，
 +
* 海马的 Schaffer 侧枝突触
   −
[[Phosphatidylinositol#Phosphoinositides|Phosphoinositides]] ([[Phosphatidylinositol 4-phosphate|PIP]], PIP2, and [[Phosphatidylinositol (3,4,5)-trisphosphate|PIP3]]) are molecules that have been shown to affect neuronal polarity.<ref name=":13">{{cite journal |last1=Arimura |first1=Nariko |last2=Kaibuchi |first2=Kozo |date=December 22, 2005 |title=Key regulators in neuronal polarity |journal=[[Neuron (journal)|Neuron]] |volume=48 |issue=6 |pages=881–884 |location=Cambridge, MA |publisher=Cell Press |pmid=16364893 |doi=10.1016/j.neuron.2005.11.007 |doi-access=free }}</ref> A gene (''ttx-7'') was identified in ''[[Caenorhabditis elegans]]'' that encodes ''myo''-inositol monophosphatase (IMPase), an enzyme that produces [[inositol]] by [[dephosphorylation|dephosphorylating]] [[inositol phosphate]]. Organisms with mutant ''ttx-7'' genes demonstrated behavioral and localization defects, which were rescued by expression of IMPase. This led to the conclusion that IMPase is required for the correct localization of synaptic protein components.<ref name="SynapticPolarity">{{cite journal |last1=Kimata |first1=Tsubasa |last2=Tanizawa |first2=Yoshinori |last3=Can |first3=Yoko |last4=Ikeda |first4=Shingo |last5=Kuhara |first5=Atsushi |last6=Mori |first6=Ikue |date=June 1, 2012 |title=Synaptic Polarity Depends on Phosphatidylinositol Signaling Regulated by myo-Inositol Monophosphatase in Caenorhabditis elegans |journal=[[Genetics (journal)|Genetics]] |volume=191 |issue=2 |pages=509–521 |location=Bethesda, MD |publisher=[[Genetics Society of America]] |pmid=22446320 |doi=10.1534/genetics.111.137844 |display-authors=3 |pmc=3374314}}</ref><ref name=":14">{{cite journal |last1=Tanizawa |first1=Yoshinori |last2=Kuhara |first2=Atsushi |last3=Inada |first3=Hitoshi |last4=Kodama |first4=Eiji |last5=Mizuno |first5=Takafumi |last6=Mori |first6=Ikue |date=December 1, 2006 |title=Inositol monophosphatase regulates localization of synaptic components and behavior in the mature nervous system of C. elegans |journal=[[Genes & Development]] |volume=20 |issue=23 |pages=3296–3310 |location=Cold Spring Harbor, NY |publisher=[[Cold Spring Harbor Laboratory Press]] |pmid=17158747 |pmc=1686606 |doi=10.1101/gad.1497806 |display-authors=3}}</ref> The ''egl-8'' gene encodes a homolog of [[phospholipase C]]β (PLCβ), an enzyme that cleaves PIP2. When ''ttx-7'' mutants also had a mutant ''egl-8'' gene, the defects caused by the faulty ''ttx-7'' gene were largely reversed. These results suggest that PIP2 signaling establishes polarized localization of synaptic components in living neurons.<ref name="SynapticPolarity" />
+
==突触极性==
 +
神经元的功能依赖于细胞极性。神经细胞独特的结构使得动作电位可以单向传递（从树突到细胞体再到轴突) ，这些信号可以被突触后神经元接收和传递，或者被效应细胞接收。长期以来，神经细胞一直被用作细胞极性的模型，尤其用来研究突触分子极性定位的机制。受肌醇单磷酸酶（IMPase） 调节的 PIP2 信号通路在突触极性中起着重要作用。
   −
磷脂酰肌醇(PIP、 pip2和 PIP3)是已被证明影响神经元极性的分子.<ref name=":13" /> 。一个基因(ttx-7)在秀丽隐桿线虫中被鉴定，它编码肌醇单磷酸酶(IMPase) ，一种通过磷酸肌醇脱磷酸化产生肌醇的酶。有 ttx-7基因突变的生物表现出行为和定位缺陷，这些缺陷是由 IMPase 的表达所拯救的。这导致了结论，IMPase 是必要的正确定位突触蛋白质成分.<ref name="SynapticPolarity" /><ref name=":14" /> 。Egl-8基因编码磷脂酶 Cβ (PLCβ)的同源基因。当 ttx-7突变体也有一个突变的 egl-8基因时，由 ttx-7基因缺陷引起的缺陷大部分被逆转。这些结果表明，pip2信号通路建立了活体神经元突触成分的极化定位.<ref name="SynapticPolarity" />。
+
磷脂酰肌醇（PIP、PIP2 和 PIP3）已被证明是影响神经元极性的分子<ref name=":13">{{cite journal |last1=Arimura |first1=Nariko |last2=Kaibuchi |first2=Kozo |date=December 22, 2005 |title=Key regulators in neuronal polarity |journal=[[Neuron (journal)|Neuron]] |volume=48 |issue=6 |pages=881–884 |location=Cambridge, MA |publisher=Cell Press |pmid=16364893 |doi=10.1016/j.neuron.2005.11.007 |doi-access=free }}</ref> 。在秀丽线虫中鉴定的基因 ttx-7，编码 IMPase——一种使磷酸肌醇脱磷酸化产生肌醇的酶。ttx-7 基因突变的线虫表现出行为和蛋白定位缺陷，而这些缺陷是通过表达 IMPase 而恢复。这些可以得出，IMPase 对突触组成蛋白的正确定位是必要的<ref name="SynapticPolarity">{{cite journal |last1=Kimata |first1=Tsubasa |last2=Tanizawa |first2=Yoshinori |last3=Can |first3=Yoko |last4=Ikeda |first4=Shingo |last5=Kuhara |first5=Atsushi |last6=Mori |first6=Ikue |date=June 1, 2012 |title=Synaptic Polarity Depends on Phosphatidylinositol Signaling Regulated by myo-Inositol Monophosphatase in Caenorhabditis elegans |journal=[[Genetics (journal)|Genetics]] |volume=191 |issue=2 |pages=509–521 |location=Bethesda, MD |publisher=[[Genetics Society of America]] |pmid=22446320 |doi=10.1534/genetics.111.137844 |display-authors=3 |pmc=3374314}}</ref><ref name=":14">{{cite journal |last1=Tanizawa |first1=Yoshinori |last2=Kuhara |first2=Atsushi |last3=Inada |first3=Hitoshi |last4=Kodama |first4=Eiji |last5=Mizuno |first5=Takafumi |last6=Mori |first6=Ikue |date=December 1, 2006 |title=Inositol monophosphatase regulates localization of synaptic components and behavior in the mature nervous system of C. elegans |journal=[[Genes & Development]] |volume=20 |issue=23 |pages=3296–3310 |location=Cold Spring Harbor, NY |publisher=[[Cold Spring Harbor Laboratory Press]] |pmid=17158747 |pmc=1686606 |doi=10.1101/gad.1497806 |display-authors=3}}</ref> 。Egl-8 基因编码磷脂酶 Cβ（PLCβ）的同源基因。当 ttx-7 突变体也发生 egl-8 基因突变时，由 ttx-7 基因突变导致的的缺陷表型可以很大程度被逆转。这些结果表明，PIP2 信号通路建立了神经元中突触组成蛋白的极性定位.<ref name="SynapticPolarity" />。
   −
== Presynaptic modulation 突触前调制 ==
+
== 突触前调制 ==
 
Modulation of neurotransmitter release by [[G protein-coupled receptor|G-protein-coupled receptors]] (GPCRs) is a prominent presynaptic mechanism for regulation of [[Neurotransmission|synaptic transmission]]. The activation of GPCRs located at the presynaptic terminal, can decrease the probability of neurotransmitter release. This presynaptic depression involves activation of [[Gi alpha subunit|Gi/o]]-type [[G protein|G-proteins]] that mediate different inhibitory mechanisms, including inhibition of [[voltage-gated calcium channel]]s, activation of [[potassium channel]]s, and direct inhibition of the [[vesicle fusion]] process. [[Cannabinoid#Endocannabinoids|Endocannabinoids]], synthesized in and released from postsynaptic [[neuron]]al elements, and their cognate [[Receptor (biochemistry)|receptors]], including the (GPCR) [[Cannabinoid receptor type 1|CB1 receptor]], located at the presynaptic terminal, are involved in this modulation by an [[retrograde signaling]] process, in which these compounds are synthesized in and released from postsynaptic neuronal elements, and travel back to the presynaptic terminal to act on the CB1 receptor for short-term (STD) or long-term synaptic depression (LTD), that cause a short or long lasting decrease in neurotransmitter release.<ref name=":15">{{Citation|last=Lovinger|first=David M.|chapter=Presynaptic Modulation by Endocannabinoids|date=2008|pages=435–477|editor-last=Südhof|editor-first=Thomas C.|series=Handbook of Experimental Pharmacology|publisher=Springer Berlin Heidelberg|language=en|doi=10.1007/978-3-540-74805-2_14|pmid=18064422|isbn=9783540748052|editor2-last=Starke|editor2-first=Klaus|title=Pharmacology of Neurotransmitter Release|volume=184|issue=184}}</ref>
 
Modulation of neurotransmitter release by [[G protein-coupled receptor|G-protein-coupled receptors]] (GPCRs) is a prominent presynaptic mechanism for regulation of [[Neurotransmission|synaptic transmission]]. The activation of GPCRs located at the presynaptic terminal, can decrease the probability of neurotransmitter release. This presynaptic depression involves activation of [[Gi alpha subunit|Gi/o]]-type [[G protein|G-proteins]] that mediate different inhibitory mechanisms, including inhibition of [[voltage-gated calcium channel]]s, activation of [[potassium channel]]s, and direct inhibition of the [[vesicle fusion]] process. [[Cannabinoid#Endocannabinoids|Endocannabinoids]], synthesized in and released from postsynaptic [[neuron]]al elements, and their cognate [[Receptor (biochemistry)|receptors]], including the (GPCR) [[Cannabinoid receptor type 1|CB1 receptor]], located at the presynaptic terminal, are involved in this modulation by an [[retrograde signaling]] process, in which these compounds are synthesized in and released from postsynaptic neuronal elements, and travel back to the presynaptic terminal to act on the CB1 receptor for short-term (STD) or long-term synaptic depression (LTD), that cause a short or long lasting decrease in neurotransmitter release.<ref name=":15">{{Citation|last=Lovinger|first=David M.|chapter=Presynaptic Modulation by Endocannabinoids|date=2008|pages=435–477|editor-last=Südhof|editor-first=Thomas C.|series=Handbook of Experimental Pharmacology|publisher=Springer Berlin Heidelberg|language=en|doi=10.1007/978-3-540-74805-2_14|pmid=18064422|isbn=9783540748052|editor2-last=Starke|editor2-first=Klaus|title=Pharmacology of Neurotransmitter Release|volume=184|issue=184}}</ref>
   −
G 蛋白偶联受体对神经递质释放的调节是突触前调节突触传递的重要机制。GPCRs 位于突触前末端，激活 GPCRs 可以降低神经递质释放的概率。这种突触前抑制涉及 Gi/o 型 g 蛋白的激活，介导不同的抑制机制，包括抑制电压门控性钙通道，激活钾通道，直接抑制囊泡融合过程。突触后神经元合成和释放的内源性大麻素及其同源受体，包括位于突触前端的(GPCR) cb1受体，通过逆行信号传导过程参与了这种调节，这些化合物在突触后神经元合成和释放，然后回到突触前端作用于短期(STD)或长期突触抑制(LTD) ，导致短期或长期神经递质释放减少。<ref name=":15" />
+
通过 G 蛋白偶联受体（GPCR）对神经递质释放进行调节是突触传递的主要突触前机制。GPCR 位于突触前末端，激活 GPCRs 可以降低神经递质释放的概率。这种突触前抑制涉及 Gi/o 型的 G 蛋白的激活，介导不同的抑制机制，包括抑制电压门控钙离子通道、激活钾离子通道，或直接抑制囊泡融合过程。内源性大麻素在突触后神经元合成和释放，通过逆向信号通路，作用于突触前膜的同源受体，比如 CB1 受体，引起短期（STD）或长期的突触抑制（LTD），导致短期或长期神经递质释放减少<ref name=":15" />。
    
==Additional images ==
 
==Additional images ==
第150行： 第95行：  
* 免疫突触  
 
* 免疫突触  
 
* 神经递质小泡  
 
* 神经递质小泡  
−
* 突触后密度
  −
* 突触病变
      
==References==
 
==References==
Okxy
99

个编辑

取自“https://wiki.swarma.org/index.php/特殊:移动版差异/31262”