Synaptic targets: Chronic alcohol actions

被引：110
作者：
Roberto, Marisa [1 ]
Varodayan, Florence P. [1 ]
机构：
[1] Scripps Res Inst, La Jolla, CA 92037 USA
来源：
NEUROPHARMACOLOGY | 2017年 / 122卷
关键词：
Alcohol/ethanol; GABA; Glutamate; Synaptic transmission; Presynaptic; Postsynaptic; Protein phosphorylation; Intoxication; Tolerance; Dependence; CHRONIC ETHANOL EXPOSURE; GAMMA-AMINOBUTYRIC-ACID; CHRONIC INTERMITTENT ETHANOL; D-ASPARTATE RECEPTORS; RAT CENTRAL AMYGDALA; PROTEIN-KINASE-A; CEREBELLAR PURKINJE NEURONS; CULTURED CORTICAL-NEURONS; VENTRAL TEGMENTAL AREA; MEDIATED EXCITATORY NEUROTRANSMISSION;
D O I：
10.1016/j.neuropharm.2017.01.013
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Alcohol acts on numerous cellular and molecular targets to regulate neuronal communication within the brain. Chronic alcohol exposure and acute withdrawal generate prominent neuroadaptations at synapses, including compensatory effects on the expression, localization and function of synaptic proteins, channels and receptors. The present article reviews the literature describing the synaptic effects of chronic alcohol exposure and their relevance for synaptic transmission in the central nervous system. This review is not meant to be comprehensive, but rather to highlight the effects that have been observed most consistently and that are thought to contribute to the development of alcohol dependence and the negative aspects of withdrawal. Specifically, we will focus on the major excitatory and inhibitory neurotransmitters in the brain, glutamate and GABA, respectively, and how their neuroadaptations after chronic alcohol exposure contributes to alcohol reinforcement, dependence and withdrawal. This article is part of the Special Issue entitled "Alcoholism". (C) 2017 Elsevier Ltd. All rights reserved.
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收藏
页码：85 / 99
页数：15
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