CLINICAL TRIAL: MEASUREMENT OF DOPAMINE SYSTEMS IN SUBJECTS AT-RISK FOR ALCOHOL

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得主要资金， 因此可以在其他CRISP条目中表示。列出的机构是 研究中心，而研究中心不一定是研究者所在的机构。 比较HR和LR（低风险）受试者的局部脑葡萄糖代谢。 我们假设，HR受试者酗酒的一个脆弱因素是OFC活性下降，因为该区域与包括酗酒在内的成瘾行为的缺乏控制和强迫性药物消费特征有关。比较酒精中毒高风险（HR）和酒精中毒低风险（LR）受试者的D2-R可用性。 我们假设，高D2-R是高血压受试者酒精中毒的保护因素，我们假设通过调节大脑奖赏回路对酒精中毒的反应来保护他们免受酒精中毒的影响，比较急性酒精给药（0.75 g/kg）引起的局部代谢变化，并评估D2-R在高血压和低血压受试者对急性酒精中毒反应中的影响。 我们假设，与低风险酗酒（LR）（酒精中毒家族史阴性）的受试者相比，HR受试者对酒精中毒的行为和局部脑代谢反应降低。 我们进一步假设，酒精诱导的代谢和行为的影响将调制的D2-R水平和活性的OFC。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for 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.