Ethanol tolerance and synaptic plasticity
Ethanol tolerance and synaptic plasticity
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DOI：
10.1016/s0165-6147(98)01268-1
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发表时间：
1998-12-01
影响因子：
13.8
通讯作者：
Crews, FT
中科院分区：
文献类型：
--
作者：
Chandler, LJ;Harris, RA;Crews, FT
目前关于乙醇对中枢神经系统的许多药理作用的机制的概念包括通过乙醇与通道亚单位蛋白上特定疏水位置的相互作用来破坏离子通道功能。临床上尤其重要的是对乙醇的耐受性和依赖性的发展，很可能是突触功能的适应性变化响应乙醇对离子通道的作用在这一过程中发挥作用。在这篇文章中，Judson Chandler，Adron Harris和Fulton团队讨论了乙醇诱导突触功能改变的潜在机制，这可能为乙醇耐受和依赖提供细胞学基础。目前认为，NMDA和GABA(A)受体涉及多种机制，包括转录和过去翻译修饰。
Current concepts of the mechanisms underlying many of the pharmacological effects of ethanol on the CNS involve disruption of ion channel function via the interaction of ethanol with specific hydrophobic sites on channel subunit proteins. Of particular clinical importance is the development of tolerance and dependence to ethanol, and it is likely that adaptive changes in synaptic function in response to ethanol's actions on ion channels play a role in this process. In this article, Judson Chandler, Adron Harris and Fulton Crews discuss potential mechanisms of ethanol-induced changes in synaptic function that might provide a cellular basis for ethanol tolerance and dependence. It is proposed that multiple mechanisms are involved that include both transcriptional and past-translational modifications in NMDA and GABA(A) receptors.