NEURAL BASIS OF THE BEHAVIORAL EFFECTS OF ALCOHOL

酒精中毒的神经基础尚不清楚。最近的研究表明 专注于酒精与氨基酸神经传递的相互作用 重要的行动地点。虽然GABA调节的氯化物的增强 渠道受到最多研究关注，有新数据 显示酒精减弱了N-甲基-D-天冬氨酸的激活 兴奋性谷氨酸受体(NMDA)亚型。该计划的目的是 建议的研究是调查以下假设：NMDA的调制- 受体介导的兴奋在急性行为效应中发挥作用 乙醇。乙醇对大鼠的歧视性刺激作用将起作用 作为急性酒精中毒的模型。它的效果将被比较和 与其他竞争性和非竞争性NMDA的对比 对抗者。此外，乙醇拮抗这些效应的能力 NMDA在体内的含量也将被确定。在重要的方面 建议的研究是将最新的生物化学技术纳入该项目 和电生理学在快速扩张的领域的发展 NMDA研究，特别是与乙醇作用有关的研究。目标是 是对令人兴奋的新发展的相关性进行评估 在神经科学中使用动物来研究酒精对行为的影响 与酒精的使用和滥用有关的属性模型 被人类发现。对酒精行为的神经基础有更多的了解 效应将为研究个体差异开辟新的机会 对酒精的遗传易感性，可能发展为生物学上的 酒精中毒的标志物，并开发酒精的新药物疗法 施虐者。

The neural basis for alcohol intoxication is unknown. Recent research has focused on alcohol's interaction with amino acid neurotransmission as an important site of action. Although enhancement of GABA-regulated chloride channels has received the most research attention, there is new data showing that alcohol attenuates the activation of the N-methyl-D-aspartate (NMDA) subtype of excitatory glutamate receptor. The purpose of the proposed research is to investigate the hypothesis that modulation of NMDA- receptor mediated excitation plays a role in the acute behavioral effects of ethanol. Ethanol's discriminative stimulus effects in rats will serve as a model of acute alcohol intoxication. It's effects will be compared and contrasted to those of other competitive and noncompetitive NMDA antagonists. In addition, the ability of ethanol to antagonize the effects of NMDA in vivo will also be determined. In important aspect of the proposed research is to incorporate into the project the latest biochemical and electrophysiological developments in the rapidly-expanding field of NMDA research, especially those related to the actions of ethanol. The goal is to provide an assessment of the relevance of exciting new developments in the neurosciences to the behavioral effects of alcohol using animal models for the properties of alcohol that are relevant to its use and abuse by humans. Greater knowledge of the neural basis for alcohol's behavioral effects will open up new opportunities to study individual differences in genetic vulnerability to alcoholisin, to possibly develop biological markers for alcoholism, and to develop novel pharmacotherapies for alcohol abusers.