Department of Psychology, Lycoming College, One College Place, Williamsport, PA, 17701, United States.
Department of Psychology, Lycoming College, One College Place, Williamsport, PA, 17701, United States.
Alcohol. 2021 Mar;91:61-73. doi: 10.1016/j.alcohol.2020.12.004. Epub 2021 Jan 9.
The rising popularity of alcohol mixed with energy drinks (AmEDs) has become a significant public health concern, with AmED users reporting higher levels of alcohol intake than non-AmED users. One mechanism proposed to explain this heightened level of alcohol intake in AmED users is that the high levels of caffeine found in energy drinks may increase the positive reinforcing properties of alcohol, an effect that may be dependent on interactions between adenosine receptor signaling pathways and the dopamine D receptor. Therefore, the purpose of the current study was to confirm whether caffeine does increase the positive reinforcing effects of alcohol using both fixed ratio (FR) and progressive ratio (PR) designs, and to investigate a potential role of the dopamine D receptor to caffeine-induced increases in alcohol self-administration. Male Long-Evans rats were trained to self-administer a sweetened alcohol solution (10% v/v alcohol + 2% w/v sucrose) on an FR2 schedule of reinforcement, and the effects of caffeine (0, 5, 10, and 20 mg/kg, i. p. [intraperitoneally]) on the maintenance of alcohol self-administration and alcohol break point were examined. Parallel experiments in rats trained to self-administer sucrose (0.8% w/v) were conducted to determine whether caffeine's reinforcement-enhancing effects extended to a non-drug reinforcer. Caffeine pretreatment (5-10 mg/kg) significantly increased sweetened alcohol self-administration and motivation for a sweetened alcohol reinforcer. However, similar increases in self-administration of a non-drug reinforcer were not observed. Contrary to our hypothesis, the D receptor antagonist eticlopride did not block a caffeine-induced increase in sweetened alcohol self-administration, nor did it alter caffeine-induced increases in motivation for a sweetened alcohol reinforcer. Taken together, these results support the hypothesis that caffeine increases the positive reinforcing effects of alcohol, which may explain caffeine-induced increases in alcohol intake. However, the reinforcement-enhancing effects of caffeine appear to be independent of D receptor function.
酒精混合能量饮料（AmEDs）的日益普及已成为一个重大的公共卫生关注点，AmED 用户报告的酒精摄入量高于非 AmED 用户。一种解释 AmED 用户中这种更高水平酒精摄入的机制是，能量饮料中发现的高浓度咖啡因可能会增加酒精的正强化特性，这种效应可能依赖于腺苷受体信号通路和多巴胺 D 受体之间的相互作用。因此，本研究的目的是使用固定比率（FR）和递增比率（PR）设计来确认咖啡因是否确实会增加酒精的正强化作用，并研究多巴胺 D 受体在咖啡因诱导的酒精自我给药增加中的潜在作用。雄性长耳大仓鼠被训练在 FR2 强化方案下自我给予加糖酒精溶液（10% v/v 酒精+2% w/v 蔗糖），并研究咖啡因（0、5、10 和 20 mg/kg，ip）对酒精自我给药的维持和酒精突破点的影响。在训练大鼠自我给予蔗糖（0.8% w/v）的平行实验中，确定咖啡因的强化增强作用是否扩展到非药物强化物。咖啡因预处理（5-10 mg/kg）显著增加了加糖酒精的自我给药和对加糖酒精强化物的动机。然而，没有观察到对非药物强化物的自我给药的类似增加。与我们的假设相反，D 受体拮抗剂 eticlopride 既不能阻断咖啡因对加糖酒精自我给药的增加，也不能改变咖啡因对加糖酒精强化物的动机增加。综上所述，这些结果支持咖啡因增加酒精正强化作用的假设，这可以解释咖啡因诱导的酒精摄入量增加。然而，咖啡因的强化作用似乎独立于 D 受体功能。
