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 which may be dependent on interactions between adenosine receptor signaling pathways and the dopamine D₂ 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 D₂ 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.) 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 if 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 D₂ 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 D₂ receptor function.

酒精混合能量饮料 (AmEDs) 的日益流行已成为一个重要的公共健康问题，AmED 用户报告的酒精摄入量高于非 AmED 用户。提出的解释 AmED 用户酒精摄入量增加的一种机制是能量饮料中发现的高水平咖啡因可能会增加酒精的积极增强特性，这种作用可能取决于腺苷受体信号通路和多巴胺之间的相互作用D ₂受体。因此，本研究的目的是使用固定比率 (FR) 和渐进比率 (PR) 设计来确认咖啡因是否确实增加了酒精的积极增强作用，并研究了多巴胺 D ₂的潜在作用咖啡因诱导的酒精自我管理增加的受体。雄性 Long Evans 大鼠经过训练，可以按照 FR2 强化计划和咖啡因（0、5、10 和 20 毫克）的效果自我给药加糖酒精溶液（10% v/v 酒精 + 2% w/v 蔗糖） /kg, ip) 对酒精自我给药的维持和酒精断点进行了检查。在训练为自我给药蔗糖 (0.8% w/v) 的大鼠中进行平行实验，以确定咖啡因的强化增强作用是否扩展到非药物强化剂。咖啡因预处理 (5-10 mg/kg) 显着增加了甜酒的自我管理和甜酒强化剂的动机。然而，没有观察到非药物强化剂自我给药的类似增加。与我们的假设相反，D ₂受体拮抗剂依替洛必利不会阻止咖啡因诱导的甜酒精自我给药增加，也不会改变咖啡因诱导的甜酒精强化剂动机增加。总之，这些结果支持咖啡因增加酒精的积极增强作用的假设，这可以解释咖啡因诱导的酒精摄入量增加。然而，咖啡因的强化增强作用似乎与 D ₂受体功能无关。