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代谢型谷氨酸受体在中枢突触处离子型谷氨酸受体和γ-氨基丁酸A受体转运中的作用

Metabotropic glutamate receptors in the trafficking of ionotropic glutamate and GABA(A) receptors at central synapses.

作者信息

Xiao Min-Yi, Gustafsson Bengt, Niu Yin-Ping

机构信息

Institute of Physiology and Pharmacology, Göteborg University, Box 432, 405 30 Göteborg, Sweden.

出版信息

Curr Neuropharmacol. 2006 Jan;4(1):77-86. doi: 10.2174/157015906775202986.

DOI:10.2174/157015906775202986
PMID:18615134
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2430676/
Abstract

The trafficking of ionotropic glutamate (AMPA, NMDA and kainate) and GABA(A) receptors in and out of, or laterally along, the postsynaptic membrane has recently emerged as an important mechanism in the regulation of synaptic function, both under physiological and pathological conditions, such as information processing, learning and memory formation, neuronal development, and neurodegenerative diseases. Non-ionotropic glutamate receptors, primarily group I metabotropic glutamate receptors (mGluRs), co-exist with the postsynaptic ionotropic glutamate and GABA(A) receptors. The ability of mGluRs to regulate postsynaptic phosphorylation and Ca(2+) concentration, as well as their interactions with postsynaptic scaffolding/signaling proteins, makes them well suited to influence the trafficking of ionotropic glutamate and GABA(A) receptors. Recent studies have provided insights into how mGluRs may impose such an influence at central synapses, and thus how they may affect synaptic signaling and the maintenance of long-term synaptic plasticity. In this review we will discuss some of the recent progress in this area: i) long-term synaptic plasticity and the involvement of mGluRs; ii) ionotropic glutamate receptor trafficking and long-term synaptic plasticity; iii) the involvement of postsynaptic group I mGluRs in regulating ionotropic glutamate receptor trafficking; iv) involvement of postsynaptic group I mGluRs in regulating GABA(A) receptor trafficking; v) and the trafficking of postsynaptic group I mGluRs themselves.

摘要

离子型谷氨酸(AMPA、NMDA和海人酸)受体以及GABA(A)受体在突触后膜内外的转运或沿突触后膜的侧向转运,最近已成为在生理和病理条件下(如信息处理、学习和记忆形成、神经元发育及神经退行性疾病)调节突触功能的重要机制。非离子型谷氨酸受体,主要是I组代谢型谷氨酸受体(mGluRs),与突触后离子型谷氨酸受体和GABA(A)受体共存。mGluRs调节突触后磷酸化和Ca(2+)浓度的能力,以及它们与突触后支架/信号蛋白的相互作用,使其非常适合影响离子型谷氨酸受体和GABA(A)受体的转运。最近的研究深入探讨了mGluRs如何在中枢突触施加这种影响,以及它们如何影响突触信号传导和长期突触可塑性的维持。在本综述中,我们将讨论该领域的一些最新进展:i)长期突触可塑性及mGluRs的参与;ii)离子型谷氨酸受体转运与长期突触可塑性;iii)突触后I组mGluRs在调节离子型谷氨酸受体转运中的作用;iv)突触后I组mGluRs在调节GABA(A)受体转运中的作用;v)突触后I组mGluRs自身的转运。

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