This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.To compare regional brain glucose metabolism in HR and LR (low-risk) subjects. We hypothesize that a vulnerability factor for alcoholism in HR subjects is decreased OFC activity since this region is implicated in the lack of control and compulsive drug consumption characteristic of addictions including alcoholism. To compare D2-R availability in subjects with high risk (HR) for alcoholism and low risk (LR) for alcoholism. We hypothesize that a protective factor for alcoholism in HR subjects is due to high D2-R, which we postulate protects them against alcoholism by regulating the response of brain reward circuits to alcohol intoxication.To compare the regional metabolic changes induced by acute alcohol administration (0.75 g/kg) and to evaluate the influence of D2-R in the responses to acute alcohol intoxication between HR and LR subjects. We hypothesize that HR subjects will have reduced behavioral and regional brain metabolic responses to alcohol intoxication when compared with subjects at low risk for alcoholism (LR) (negative family history of alcoholism). We further hypothesize that alcohol-induced metabolic and behavioral effects will be modulated by D2-R levels and activity in OFC.
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