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This hypothesis was grounded in the observations that alcohol-elicited place conditioning is prevented by DA receptor antagonists [15, 16], that caffeine exerts, through an antagonistic action on A 2A adenosine receptors (A 2A R) [17], a direct negative control on neuronal firing of DA cells in the posterior ventral tegmental area (pVTA) [18], and that caffeine administration prior to alcohol also prevents its DA-dependent [19] ability to increase the expression of phosphorylated Extracellular signal Regulated Kinase (pERK) in the shell of the nucleus accumbens (AcbSh) [13, 20]