Ferré Sergi, O'Brien Mary Claire
CNS Receptor-Receptor Interactions Unit, National Institute on Drug Abuse , Intramural Research Program, Department of Health and Human Services, Baltimore, Maryland.
Department of Emergency Medicine, Wake Forest School of Medicine , Winston-Salem, North Carolina. ; Department of Social Sciences & Health Policy, Wake Forest School of Medicine , Winston-Salem, North Carolina.
J Caffeine Res. 2011 Sep;1(3):153-162. doi: 10.1089/jcr.2011.0017.
Although it is widely believed that caffeine antagonizes the intoxicating effects of alcohol, the molecular mechanisms underlying their interaction are incompletely understood. It is known that both caffeine and alcohol alter adenosine neurotransmission, but the relationship is complex, and may be dose dependent. In this article, we review the available literature on combining caffeine and alcohol. Ethical constraints prohibit laboratory studies that would mimic the high levels of alcohol intoxication achieved by many young people in real-world settings, with or without the addition of caffeine. We propose a possible neurochemical mechanism for the increase in alcohol consumption and alcohol-related consequences that have been observed in persons who simultaneously consume caffeine. Caffeine is a nonselective adenosine receptor antagonist. During acute alcohol intake, caffeine antagonizes the "unwanted" effects of alcohol by blocking the adenosine A receptors that mediate alcohol's somnogenic and ataxic effects. The A receptor-mediated "unwanted" anxiogenic effects of caffeine may be ameliorated by alcohol-induced increase in the extracellular concentration of adenosine. Moreover, by means of interactions between adenosine A and dopamine D receptors, caffeine-mediated blockade of adenosine A receptors can potentiate the effects of alcohol-induced dopamine release. Chronic alcohol intake decreases adenosine tone. Caffeine may provide a "treatment" for the withdrawal effects of alcohol by blocking the effects of upregulated A receptors. Finally, blockade of A receptors by caffeine may contribute to the reinforcing effects of alcohol.
尽管人们普遍认为咖啡因能对抗酒精的醉酒作用，但其相互作用的分子机制尚未完全明了。已知咖啡因和酒精都会改变腺苷神经传递，但这种关系很复杂，可能还取决于剂量。在本文中，我们综述了有关咖啡因与酒精联用的现有文献。伦理限制禁止进行实验室研究，这类研究无法模拟许多年轻人在现实环境中达到的高度酒精中毒状态，无论是否添加咖啡因。我们提出了一种可能的神经化学机制，来解释在同时摄入咖啡因的人群中观察到的酒精消费量增加及与酒精相关后果。咖啡因是一种非选择性腺苷受体拮抗剂。在急性酒精摄入期间，咖啡因通过阻断介导酒精催眠和共济失调作用的腺苷A受体，对抗酒精的“不良”作用。酒精诱导的细胞外腺苷浓度升高，可能会减轻咖啡因由A受体介导的“不良”焦虑作用。此外，通过腺苷A受体和多巴胺D受体之间的相互作用，咖啡因介导的腺苷A受体阻断作用可增强酒精诱导的多巴胺释放效应。长期摄入酒精会降低腺苷张力。咖啡因可能通过阻断上调的A受体的作用，为酒精戒断效应提供一种“治疗”方法。最后，咖啡因对A受体的阻断作用可能会增强酒精的强化作用。
