Synaptic effects induced by alcohol.
Synaptic effects induced by alcohol.
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酒精引起的突触作用。
DOI：
10.1007/7854_2011_143
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发表时间：
2013
影响因子：
--
通讯作者：
Roberto M
中科院分区：
文献类型：
--
作者：
Lovinger DM;Roberto M
乙醇（EtOH）对许多细胞分子靶点有影响，突触功能的改变在这些影响中是突出的。急性暴露于EtOH激活或抑制参与突触传递的蛋白质的功能，而慢性暴露通常对这些蛋白质的表达、定位和功能产生相反和/或补偿/稳态效应。不同神经递质之间的相互作用（例如，神经肽对小分子递质释放的影响）也可以影响急性和慢性EtOH作用。对完整动物的研究表明，受EtOH影响的蛋白质也在药物的神经作用中发挥作用，包括急性中毒、耐受性、依赖性以及寻找和饮用EtOH。本章回顾了描述乙醇的急性和慢性突触效应及其与突触传递、可塑性和行为的相关性的文献。
Ethanol (EtOH) has effects on numerous cellular molecular targets, and alterations in synaptic function are prominent among these effects. Acute exposure to EtOH activates or inhibits the function of proteins involved in synaptic transmission, while chronic exposure often produces opposing and/or compensatory/homeostatic effects on the expression, localization, and function of these proteins. Interactions between different neurotransmitters (e.g., neuropeptide effects on release of small molecule transmitters) can also influence both acute and chronic EtOH actions. Studies in intact animals indicate that the proteins affected by EtOH also play roles in the neural actions of the drug, including acute intoxication, tolerance, dependence, and the seeking and drinking of EtOH. This chapter reviews the literature describing these acute and chronic synaptic effects of EtOH and their relevance for synaptic transmission, plasticity, and behavior.