While a recent study found greater ventral striatum activation to alcohol cues in social drinkers and greater dorsal striatum activation to alcohol cues in heavy drinkers (Vollstadt-Klein et al., 2010), alcoholism severity was controlled for in the present study. Controlling for severity allowed us to more effectively test the effects of genotype at matched levels of clinical impairment. As such, the present findings do not address the role of clinical severity on ventral versus dorsal striatum connectivity and instead focus on the role of the A118G SNP to these putative risk pathways for alcoholism. To that end, whole brain analyses suggest that the G-allele of the OPRM1 gene is associated with (a) greater activation of opioid receptor rich areas of the brain (insula, OFC) and (b) negative fronto-striatal functional connectivity in both ventral and dorsal striatum during processing of alcohol cues. These findings suggest that inhibition of reward and/or habit-driven inputs from the striatum by the prefrontal control circuitry may be unstable among G-allele carriers. Importantly, the G-allele could show similar instability in fronto-striatal connectivity to other cues with incentive
