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神经元中内吞作用与外排作用偶联的分子机制。

Molecular Mechanisms for the Coupling of Endocytosis to Exocytosis in Neurons.

作者信息

Xie Zhenli, Long Jiangang, Liu Jiankang, Chai Zuying, Kang Xinjiang, Wang Changhe

机构信息

Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong UniversityXi'an, China; Frontier Institute of Science and Technology, Xi'an Jiaotong UniversityXi'an, China; State Key Laboratory of Membrane Biology, Peking UniversityBeijing, China; Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Institute of Molecular Medicine, Peking UniversityBeijing, China.

Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong UniversityXi'an, China; Frontier Institute of Science and Technology, Xi'an Jiaotong UniversityXi'an, China.

出版信息

Front Mol Neurosci. 2017 Mar 13;10:47. doi: 10.3389/fnmol.2017.00047. eCollection 2017.

Abstract

Neuronal communication and brain function mainly depend on the fundamental biological events of neurotransmission, including the exocytosis of presynaptic vesicles (SVs) for neurotransmitter release and the subsequent endocytosis for SV retrieval. Neurotransmitters are released through the Ca- and SNARE-dependent fusion of SVs with the presynaptic plasma membrane. Following exocytosis, endocytosis occurs immediately to retrieve SV membrane and fusion machinery for local recycling and thus maintain the homeostasis of synaptic structure and sustained neurotransmission. Apart from the general endocytic machinery, recent studies have also revealed the involvement of SNARE proteins (synaptobrevin, SNAP25 and syntaxin), synaptophysin, Ca/calmodulin, and members of the synaptotagmin protein family (Syt1, Syt4, Syt7 and Syt11) in the balance and tight coupling of exo-endocytosis in neurons. Here, we provide an overview of recent progress in understanding how these neuron-specific adaptors coordinate to ensure precise and efficient endocytosis during neurotransmission.

摘要

神经元通讯和脑功能主要依赖于神经传递的基本生物学过程,包括突触前囊泡(SVs)的胞吐作用以释放神经递质,以及随后的内吞作用以回收SVs。神经递质通过Ca2+和SNARE蛋白依赖的SVs与突触前质膜的融合而释放。胞吐作用之后,内吞作用立即发生,以回收SV膜和融合机制用于局部循环利用,从而维持突触结构的稳态和持续的神经传递。除了一般的内吞机制外,最近的研究还揭示了SNARE蛋白(突触小泡蛋白、SNAP25和 syntaxin)、突触素、Ca2+/钙调蛋白以及突触结合蛋白家族成员(Syt1、Syt4、Syt7和Syt11)参与神经元中外-内吞作用的平衡和紧密偶联。在这里,我们概述了在理解这些神经元特异性衔接蛋白如何协调以确保神经传递过程中精确而有效的内吞作用方面的最新进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/246a/5346583/e7bc082e4a2a/fnmol-10-00047-g0001.jpg

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