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−	~~本中文词条由神经动力学模型读书会词条梳理志愿者~~ okxy 翻译审校，[[用户:薄荷\|薄荷]]编辑，如有问题，欢迎在讨论页面留言。	+	本中文词条由周昌松老师提供，由神经动力学模型读书会词条梳理志愿者 okxy 翻译审校，[[用户:薄荷\|薄荷]]编辑，如有问题，欢迎在讨论页面留言。

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 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。一个例子是内源性大麻素，其在突触后神经元合成和释放，通过逆向信号通路（突触后神经元合成与释放的分子反向作用到突触前末梢），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">{{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>。
-==References ==
+==参考文献 ==
 {{Reflist|30em}}
-[[Category:待整理页面]]

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		+	此词条由神经系统中的动力学模型读书会词条梳理志愿者 okxy 翻译审校，未经专家审核，带来阅读不便，请见谅。
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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。		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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 ==References ==
 {{Reflist|30em}}
 [[Category:Signal transduction]]
 [[Category:Neural synapse| ]]
 [[Category:待整理页面]]

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 [[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]]
 ==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>。
+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>。
 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>。
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 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。一个例子是内源性大麻素，其在突触后神经元合成和释放，通过逆向信号通路（突触后神经元合成与释放的分子反向作用到突触前末梢），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">{{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>。
-==Additional images ==
+==References ==
 {{Reflist|30em}}

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 == 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>
+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。一个例子是内源性大麻素，其在突触后神经元合成和释放，通过逆向信号通路（突触后神经元合成与释放的分子反向作用到突触前末梢），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">{{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>。
 ==Additional images ==

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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>
 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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 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>
 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" />。
 ==History of the concept 概念史==
-[[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 [[Ancient Greek|Greek]] ''synapsis'' ({{lang|grc|συνάψις}}), meaning "conjunction", which in turn derives from {{lang|grc|συνάπτεὶν}} ({{lang|grc|συν}} ("together")  and {{lang|grc|ἅπτειν}} ("to fasten"))
+[[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"))
 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”))
 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>
 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" />