In light of the research implicating endogenous opioids (Heinz et al., 2005a; Ramchandani et al., 2011) and striatal dopamine (Heinz et al., 2005b; Heinz et al., 2004) in cue-induced alcohol craving, this study examines dorsal and ventral-striatal functional connectivity during alcohol cue processing as a function of OPRM1 genotype. To the extent to which the ventral striatal pathway subserves reward-driven drinking (Everitt and Robbins, 2005) and based on the literature suggesting this polymorphism is implicated in reward drinking (Ray et al., 2012), we predicted differences in ventral striatal functional connectivity as a function of OPRM1 genotype. These differences would have the potential to explain variation in reward-driven drinking between the allelic groups based on fronto-striatal connectivity. First, we hypothesized that these differences are driven by weakened frontal control over ventral striatal reward signals. This would be predicted by weaker fronto-striatal connectivity in G-allele carriers. Alternatively, stronger connectivity in G-allele carriers would suggest a greater need for frontal regulation of disproportionately greater reward sensitivity in this group. No differences in dorsal striatal connectivity were hypothesized, as this polymorphism has not been
