伏隔核
内吞作用
敏化
AMPA受体
药理学
神经科学
长时程增强
神经传递
网格蛋白
化学
突触可塑性
细胞生物学
生物
受体
NMDA受体
生物化学
中枢神经系统
作者
Karen Brebner,Tak Pan Wong,Lidong Liu,Yitao Liu,P. Campsall,Sarah L. Gray,Lindsay Phelps,Anthony G. Phillips,Yu Tian Wang
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2005-11-25
卷期号:310 (5752): 1340-1343
被引量:286
标识
DOI:10.1126/science.1116894
摘要
Drug-dependent neural plasticity related to drug addiction and schizophrenia can be modeled in animals as behavioral sensitization, which is induced by repeated noncontingent or self-administration of many drugs of abuse. Molecular mechanisms that are critical for behavioral sensitization have yet to be specified. Long-term depression (LTD) of α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor (AMPAR)–mediated synaptic transmission in the brain has been proposed as a cellular substrate for learning and memory. The expression of LTD in the nucleus accumbens (NAc) required clathrin-dependent endocytosis of postsynaptic AMPARs. NAc LTD was blocked by a dynamin-derived peptide that inhibited clathrin-mediated endocytosis or by a GluR2-derived peptide that blocked regulated AMPAR endocytosis. Systemic or intra-NAc infusion of the membrane-permeable GluR2 peptide prevented the expression of amphetamine-induced behavioral sensitization in the rat.
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