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突触可塑性机制:从膜到细胞内AMPA受体转运

Mechanisms of synaptic plasticity: from membrane to intracellular AMPAR trafficking.

作者信息

Zhu J Julius

机构信息

Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.

出版信息

Mol Interv. 2003 Feb;3(1):15-8. doi: 10.1124/mi.3.1.15.

DOI:10.1124/mi.3.1.15
PMID:14993434
Abstract

Brief periods of repetitive neural firing onto adjacent neurons can lead to changes in synaptic plasticity, that is, changes in the make-up of macromolecular complexes located at synapses. This process includes the regulated trafficking of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) to synaptic membranes. Little is known, however, about how the AMPARs are regulated before they are shuttled to the membrane. Greger et al. have found that the length of the cytoplasmic tails of constituent subunits of a given AMPAR is determined by editing [at a glutamine (Q) or an arginine (R) codon] near their C termini. Tail length, in turn, dictates whether AMPARs will be retained or quickly released from the endoplasmic reticulum.

摘要

短时间内对相邻神经元进行重复性神经放电可导致突触可塑性发生变化,即位于突触处的大分子复合物组成发生变化。这一过程包括α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体(AMPARs)向突触膜的调控转运。然而,对于AMPARs在被转运到膜之前是如何被调控的,人们知之甚少。格雷格等人发现,特定AMPAR组成亚基的细胞质尾巴长度是由其C端附近的编辑(在谷氨酰胺(Q)或精氨酸(R)密码子处)决定的。反过来,尾巴长度决定了AMPARs是会被保留在内质网中还是会迅速从内质网中释放出来。

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