BRAIN METABOLISM IN ALCOHOLICS WITH/WITHOUT CHALLENGE WITH BENZODIAZEPINE DRUG

酗酒对社会、医疗和经济的破坏性影响， 更需要了解潜在的神经化学机制 酒精自我管理和依赖。在动物和 体外系统已经产生了越来越多的证据表明，GABA- 苯二氮卓受体复合物（GBRC）介导的一些 乙醇的药理学和行为学效应，尤其是遗传学效应， 乙醇响应的可变性。此外，我们最近的研究表明， 我们在实验室中使用PET直接检查局部大脑 正常男性受试者大脑中的葡萄糖代谢， 解毒的男性酗酒者（Escherow等人，1993年）支持参与 GBRC作为酒精中毒的神经化学底物。 目的： 具体目的：1.研究GBRC介导的抑制 正常对照组和最近戒毒的酗酒者的神经传递; 具体目标2：研究饮酒时间的影响 戒断对GBRC介导的抑制性神经传递的影响; 具体目标3研究饮酒时间段的影响 在基线期间对局部脑葡萄糖代谢的影响。

The devastating social, medical, and economic effects of alcoholism have intensified the need to understand the neurochemical mechanisms underlying alcohol self administration and dependence. Studies in animals and in vitro systems have produced increasing evidence that the GABA- benzodiazepine receptor complex (GBRC) mediates some of the pharmacological and behavioral effects of ethanol, especially the genetic variability in ethanol response. Furthermore, recent studies from our laboratory in which we have used PET to directly examine regional brain glucose metabolism in the brains of normal male subjects and recently detoxified male alcoholics (Volkow et al. 1993) support the involvement of the GBRC as a neurochemical substrate in alcoholism. Purpose: Specific aim 1 To investigate the activity of GBRC mediated inhibitory neurotransmission in normal controls and recently detoxified alcoholics; Specific aim 2 To examine the influence of the time period of alcohol withdrawal on GBRC mediated inhibitory neurotransmission; Specific aim 3 To examine the influence of the time period of alcohol withdrawal on regional brain glucose metabolism during baseline.