Sanna E, Harris R A
Department of Pharmacology, University of Colorado Health Sciences Center, Denver.
Recent Dev Alcohol. 1993;11:169-86.
Effects of ethanol on ion channels were last reviewed in this series in 1987; since that time our understanding of ion channel function has advanced markedly and this explosion of knowledge has also strongly influenced studies of ethanol actions. In particular, it is now clear that there are many subtypes of ligand- and voltage-gated ion channels and that the ethanol sensitivity of these channels is subtype dependent. Among the ligand-gated ion channels, the glutamate-activated channels, particularly the NMDA subtypes, are inhibited by low concentrations of ethanol. In contrast, function of 5-HT3- and some GABA-activated channels is enhanced by acute ethanol exposure. In addition, certain voltage-dependent calcium channels are potently inhibited by ethanol. With chronic exposure, there are often compensatory changes in ion channel function that may play a role in tolerance or dependence. Genetic approaches, both classical and molecular, have proven powerful in understanding the role of ion channels in ethanol actions and are likely to figure prominently in future research in this area.
本系列上一次对乙醇对离子通道的影响进行综述是在1987年；自那时以来，我们对离子通道功能的理解有了显著进展，并且这一知识的激增也强烈影响了对乙醇作用的研究。特别是，现在很清楚的是，配体门控和电压门控离子通道有许多亚型，并且这些通道的乙醇敏感性取决于亚型。在配体门控离子通道中，谷氨酸激活的通道，尤其是NMDA亚型，会被低浓度乙醇抑制。相比之下，急性乙醇暴露会增强5-HT3和一些GABA激活通道的功能。此外，某些电压依赖性钙通道会被乙醇强烈抑制。长期暴露后，离子通道功能通常会有代偿性变化，这可能在耐受性或依赖性中起作用。经典和分子遗传学方法在理解离子通道在乙醇作用中的作用方面已被证明很强大，并且很可能在该领域未来的研究中占据突出地位。
