NEURAL BASIS OF THE BEHAVIORAL EFFECTS OF ALCOHOL

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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.