Ameisen Olivier
Am J Drug Alcohol Abuse. 2008;34(2):235-6; author reply 237-8. doi: 10.1080/00952990701877177.
It has been hypothesized that the therapeutic effects of Gamma-hydroxybutyrate (GHB) in alcohol dependence could be related to ethanol-mimicking action of the drug and that GHB could reduce alcohol craving, intake and withdrawal by acting as a "substitute" of the alcohol in the central nervous system. Nevertheless, alcohol being the strongest trigger of craving and intake, it is difficult to ascribe reduction of craving and intake to ethanol-mimicking activity of GHB. I have recently proposed that alcohol/substance dependence could result from a GHB-deficiency-related dysphoric syndrome in which alcohol/substances would be sought to "substitute" for insufficient GHB effect. GHB is the sole identified naturally occurring gamma-aminobutyric acid B (GABA (B)) receptor agonist. Here, I propose that exogenous GHB might in fact "substitute" for deficient endogeneous GHB and represent true substitutive treatment for GHB-deficiency. And that baclofen and GHB could both compensate for deficient effect of the physiological GABA (B) receptor agonist(s).
有假说认为，γ-羟基丁酸（GHB）对酒精依赖的治疗作用可能与其模拟乙醇的作用有关，并且GHB可通过在中枢神经系统中充当酒精的“替代品”来减少对酒精的渴望、摄入量及戒断反应。然而，酒精是引发渴望和摄入的最强诱因，因此很难将对渴望和摄入量的减少归因于GHB模拟乙醇的活性。我最近提出，酒精/物质依赖可能源于与GHB缺乏相关的烦躁综合征，在该综合征中，人们会寻求酒精/物质来“替代”不足的GHB效应。GHB是唯一已确定的天然存在的γ-氨基丁酸B（GABA（B））受体激动剂。在此，我提出外源性GHB实际上可能“替代”内源性GHB的不足，并代表对GHB缺乏的真正替代治疗。并且巴氯芬和GHB都可以补偿生理性GABA（B）受体激动剂的不足效应。
