突触

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25px  此article介紹的是synapses of the nervous system。For other uses, see Synapse (disambiguation).

模板:Synapse map 模板:Presynaptic synapse


In the nervous system, a synapse 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.

在神经系统中，神经元（即神经细胞）通过称为突触[1]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。

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 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. Astrocytes also exchange information with the synaptic neurons, responding to synaptic activity and, in turn, regulating neurotransmission.[2] 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.[3]

突触对于神经冲动在神经元之间传递是至关重要的。神经元是向靶细胞传递信号的特化细胞，而突触正是它们传递信号的手段。在突触，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，将前、后膜联接并执行信号传导过程。在许多突触中，突触前位于轴突，突触后位于树突或胞体上。星形胶质细胞也能对突触活动做出反应，并与形成突触的神经元交换信息，从而调节神经传递[2]。突触粘附分子（SAMs），从突触前和突触后神经元伸出，并在重叠的地方粘附在一起，从而使突触(至少是化学突触)稳定在其位置。SAMs 也可能促进突触的产生和功能执行[3]。


Some authors generalize the concept of the synapse to include the communication from a neuron to any other cell type,[4] such as to a motor cell, although such non-neuronal contacts may be referred to as junctions (a historically older term). A landmark study by Sanford Palay demonstrated the existence of synapses.[5]

有些研究者将突触的概念推展到也包括从神经元到任何其他细胞类型的通讯[4]。 例如，神经元到运动细胞的突触，尽管这种非神经元的接触可能被称为接头（一个更为早期的术语）。桑福德帕雷（Sanford Palay） 的一项具有里程碑意义的研究证明了突触的存在[5]。

History of the concept概念的历史

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.[6] The word "synapse" was introduced in 1897 by the English neurophysiologist Charles Sherrington in Michael Foster's Textbook of Physiology.[1] 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.[7][8] The word was derived from the Greek synapsis , meaning "conjunction", which in turn derives from ( ("together") and ("to fasten"))

圣地亚哥·拉蒙-卡哈尔（Santiago Ramón y Cajal）提出神经元在整个身体内并不是连续的，但仍然相互交流，这个思想被称为神经元学说.[6] 。“突触”一词是由英国神经生理学家查尔斯 · 谢林顿（Charles Sherrington）于1897年在迈克尔 · 福斯特的《生理学教科书》中提出的[1]。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 · 维拉尔建议的.[7][8] 。这个词来源于希腊语 synapsis，意思是“连接”，它又来源于“一起”和“拴牢”。


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.[9][10]

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[9][10]。

Chemical and electrical synapses电突触和化学突触

生成缩略图出错：尺寸超过12.5 MP的文件
An example of chemical synapse by the release of neurotransmitters like acetylcholine or glutamic acid.

There are two fundamentally different types of synapses:

  • In a chemical synapse, electrical activity in the presynaptic neuron is converted (via the activation of voltage-gated calcium channels) into the release of a chemical called a neurotransmitter that binds to 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: glutamatergic (often excitatory), GABAergic (often inhibitory), cholinergic (e.g. vertebrate neuromuscular junction), and adrenergic (releasing norepinephrine). Because of the complexity of receptor signal transduction, chemical synapses can have complex effects on the postsynaptic cell.
  • In an electrical synapse, the presynaptic and postsynaptic cell membranes are connected by special channels called gap junctions 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.[11]

存在两种完全不同的类型的突触：

  • 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。
  • 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。[11]


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。

An autapse is a chemical or electrical synapse that forms when the axon of one neuron synapses onto dendrites of the same neuron.

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。

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, 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。

Different types of synapses

thumb|500px|center|Different types of synapses

拇指 | 500px | 中心 | 不同类型的突触

Role in memory 记忆中的作用

Main article: 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.[12]

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[12]。


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 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.[13]

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[13]。

Study models

For technical reasons, synaptic structure and function have been historically studied at unusually large model synapses, for example:

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[14]
  • 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 potentials 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. PIP2 signaling regulated by 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。


Phosphoinositides (PIP, PIP2, and PIP3) are molecules that have been shown to affect neuronal polarity.[15] A gene (ttx-7) was identified in Caenorhabditis elegans that encodes myo-inositol monophosphatase (IMPase), an enzyme that produces inositol by 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.[16][17] The egl-8 gene encodes a homolog of phospholipase Cβ (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.[16]

磷脂酰肌醇(PIP、 pip2和 PIP3)是已被证明影响神经元极性的分子[15]。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[16][17] 。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.[16]。

Presynaptic modulation 突触前调制

Modulation of neurotransmitter release by G-protein-coupled receptors (GPCRs) is a prominent presynaptic mechanism for regulation of 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/o-type G-proteins that mediate different inhibitory mechanisms, including inhibition of voltage-gated calcium channels, activation of potassium channels, and direct inhibition of the vesicle fusion process. Endocannabinoids, synthesized in and released from postsynaptic neuronal elements, and their cognate receptors, including the (GPCR) 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.[18]

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[18]。

Additional images

  • Neuron synapse.svg

    A typical central nervous system synapse

  • Active zone3.JPG

    The synapse and synaptic vesicle cycle

  • Major elements in chemical synaptic transmission 


Image:Neuron synapse.svg|A typical central nervous system synapse
Image:Active zone3.JPG|The synapse and synaptic vesicle cycle
Image:Chemical synapse schema cropped.jpg|Major elements in chemical synaptic transmission


神经元突触 | 典型的中枢神经系统突触图像: Active zone3. jpg | The synapse and synaptic vesicle cycle 图像: 突触间隙模式 cropped.jpg | 化学突触传递的主要元素

See also 参见

模板:Col div


  • Active zone
  • Autapse
  • Exocytosis
  • Immunological synapse
  • Neurotransmitter vesicle
  • Postsynaptic density
  • Synaptopathy


  • 活动区
  • Autapse
  • 胞吐作用
  • 免疫突触
  • 神经递质小泡
  • 突触后密度
  • 突触病变

References

  1. ↑ 1.0 1.1 1.2 Foster, M.; Sherrington, C.S. (1897). Textbook of Physiology, volume 3 (7th ed.). London: Macmillan. p. 929. 
  2. ↑ 2.0 2.1 Perea, G.; Navarrete, M.; Araque, A. (August 2009). "Tripartite synapses: astrocytes process and control synaptic information". Trends in Neurosciences. Cambridge, MA: Cell Press. 32 (8): 421–431. doi:10.1016/j.tins.2009.05.001. PMID 19615761. S2CID 16355401.
  3. ↑ 3.0 3.1 Missler, M; Südhof, TC; Biederer, T (2012). "Synaptic cell adhesion". Cold Spring Harb Perspect Biol. 4 (4): a005694. doi:10.1101/cshperspect.a005694. PMC 3312681. PMID 22278667.
  4. ↑ 4.0 4.1 Schacter, Daniel L.; Gilbert, Daniel T.; Wegner, Daniel M. (2011). Psychology (2nd ed.). New York: Worth Publishers. p. 80. ISBN 978-1-4292-3719-2. LCCN 2010940234. OCLC 696604625. https://archive.org/details/psychology0000scha. 
  5. ↑ 5.0 5.1 Palay, Sanford (1956). "Synapses in the central nervous system". J Biophys Biochem Cytol. 2 (4): 193–202. doi:10.1083/jcb.2.4.193. PMC 2229686. PMID 13357542.
  6. ↑ 6.0 6.1 Elias, Lorin J.; Saucier, Deborah M. (2006). Neuropsychology: Clinical and Experimental Foundations. Boston: Pearson/Allyn & Bacon. ISBN 978-0-20534361-4. LCCN 2005051341. OCLC 61131869. 
  7. ↑ 7.0 7.1 "synapse". Online Etymology Dictionary. Archived from the original on 2013-12-14. Retrieved 2013-10-01.
  8. ↑ 8.0 8.1 Tansey, E.M. (1997). "Not committing barbarisms: Sherrington and the synapse, 1897". Brain Research Bulletin. Amsterdam: Elsevier. 44 (3): 211–212. doi:10.1016/S0361-9230(97)00312-2. PMID 9323432. S2CID 40333336. The word synapse first appeared in 1897, in the seventh edition of Michael Foster's Textbook of Physiology.
  9. ↑ 9.0 9.1 De Robertis, Eduardo D.P.; Bennett, H. Stanley (1955). "Some features of the submicroscopic morphology of synapses in frog and earthworm" (PDF). Journal of Biophysical and Biochemical Cytology. 1 (1): 47–58. doi:10.1083/jcb.1.1.47. PMC 2223594.
  10. ↑ 10.0 10.1 Palay, Sanford L.; Palade, George E. (1955). "The fine structure of neurons" (PDF). Journal of Biophysical and Biochemical Cytology. 1 (1): 69–88. doi:10.1083/jcb.1.1.69. PMC 2223597.
  11. ↑ 11.0 11.1 Silverthorn, Dee Unglaub (2007). Human Physiology: An Integrated Approach. Illustration coordinator William C. Ober; illustrations by Claire W. Garrison; clinical consultant Andrew C. Silverthorn; contributions by Bruce R. Johnson (4th ed.). San Francisco: Pearson/Benjamin Cummings. p. 271. ISBN 978-0-8053-6851-2. LCCN 2005056517. OCLC 62742632. 
  12. ↑ 12.0 12.1 Lynch, M. A. (January 1, 2004). "Long-Term Potentiation and Memory". Physiological Reviews. 84 (1): 87–136. doi:10.1152/physrev.00014.2003. PMID 14715912.
  13. ↑ 13.0 13.1 Krugers, Harm J.; Zhou, Ming; Joëls, Marian; Kindt, Merel (October 11, 2011). "Regulation of Excitatory Synapses and Fearful Memories by Stress Hormones". Frontiers in Behavioral Neuroscience. Switzerland: Frontiers Media SA. 5: 62. doi:10.3389/fnbeh.2011.00062. PMC 3190121. PMID 22013419.
  14. ↑ 14.0 14.1 Stanley, EF (1992). "The calyx-type synapse of the chick ciliary ganglion as a model of fast cholinergic transmission". Canadian Journal of Physiology and Pharmacology. 70 Suppl: S73-7. doi:10.1139/y92-246. PMID 1338300.
  15. ↑ 15.0 15.1 Arimura, Nariko; Kaibuchi, Kozo (December 22, 2005). "Key regulators in neuronal polarity". Neuron. Cambridge, MA: Cell Press. 48 (6): 881–884. doi:10.1016/j.neuron.2005.11.007. PMID 16364893.
  16. ↑ 16.0 16.1 16.2 16.3 Kimata, Tsubasa; Tanizawa, Yoshinori; Can, Yoko; et al. (June 1, 2012). "Synaptic Polarity Depends on Phosphatidylinositol Signaling Regulated by myo-Inositol Monophosphatase in Caenorhabditis elegans". Genetics. Bethesda, MD: Genetics Society of America. 191 (2): 509–521. doi:10.1534/genetics.111.137844. PMC 3374314. PMID 22446320.
  17. ↑ 17.0 17.1 Tanizawa, Yoshinori; Kuhara, Atsushi; Inada, Hitoshi; et al. (December 1, 2006). "Inositol monophosphatase regulates localization of synaptic components and behavior in the mature nervous system of C. elegans". Genes & Development. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press. 20 (23): 3296–3310. doi:10.1101/gad.1497806. PMC 1686606. PMID 17158747.
  18. ↑ 18.0 18.1 Lovinger, David M. (2008), "Presynaptic Modulation by Endocannabinoids", in Südhof, Thomas C.; Starke, Klaus (eds.), Pharmacology of Neurotransmitter Release, Handbook of Experimental Pharmacology (in English), vol. 184, Springer Berlin Heidelberg, pp. 435–477, doi:10.1007/978-3-540-74805-2_14, ISBN 9783540748052, PMID 18064422

模板:Nervous tissue

Category:Signal transduction


类别: 信号转导


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