Gianoulakis C
Douglas Hospital Research Centre, Department of Psychiatry, McGill University, Montreal, Que.
J Psychiatry Neurosci. 2001 Sep;26(4):304-18.
There is increasing evidence supporting a link between the endogenous opioid system and excessive alcohol consumption. Acute or light alcohol consumption stimulates the release of opioid peptides in brain regions that are associated with reward and reinforcement and that mediate, at least in part, the reinforcing effects of ethanol. However, chronic heavy alcohol consumption induces a central opioid deficiency, which may be perceived as opioid withdrawal and may promote alcohol consumption through the mechanisms of negative reinforcement. The role of genetic factors in alcohol dependency is well recognized, and there is evidence that the activity of the endogenous opioid system under basal conditions and in response to ethanol may play a role in determining an individual's predisposition to alcoholism. The effectiveness of opioid receptor antagonists in decreasing alcohol consumption in people with an alcohol dependency and in animal models lends further support to the view that the opioid system may regulate, either directly or through interactions with other neurotransmitters, alcohol consumption. A better understanding of the complex interactions between ethanol, the endogenous opioids and other neurotransmitter systems will help to delineate the neurochemical mechanisms leading to alcoholism and may lead to the development of novel treatments.
越来越多的证据支持内源性阿片系统与过量饮酒之间存在联系。急性或轻度饮酒会刺激与奖赏和强化相关的脑区释放阿片肽,这些脑区至少部分介导了乙醇的强化作用。然而,长期大量饮酒会导致中枢阿片缺乏,这可能被视为阿片戒断反应,并可能通过负强化机制促进饮酒。遗传因素在酒精依赖中的作用已得到充分认识,有证据表明,基础条件下以及对乙醇反应时内源性阿片系统的活性可能在决定个体对酒精成瘾的易感性方面发挥作用。阿片受体拮抗剂在减少酒精依赖者的饮酒量以及动物模型中的有效性,进一步支持了这样一种观点,即阿片系统可能直接或通过与其他神经递质的相互作用来调节饮酒行为。更好地理解乙醇、内源性阿片和其他神经递质系统之间的复杂相互作用,将有助于阐明导致酒精成瘾的神经化学机制,并可能促成新治疗方法的开发。