A secondary aim of the study was to investigate the potential moderating role of the OPRM1 gene on priming-related differences in alcohol cue-reactivity. The exploratory analysis controlling for alcoholism severity revealed greater region specific alcohol cue-elicited changes in activation between pre- and post-priming scans for G-allele carriers, as compared to the A-allele homozygotes. Specifically, the G-allele carriers exhibited greater priming related decreases in activation during alcohol cues in regions such as the left caudate, thalamus, putamen, and parietal cortex. Although the precise nature of these genotype differences remains unclear, the greater reduction in activation post-priming observed in the G-allele carriers may be related to reduced OPRM1 receptor expression, and potential subsequent reduction of receptor activation, relative to A-allele homozygotes (33, 34). The abundance of mu-opioid receptors in the thalamus, caudate nucleus, and putamen, in particular, further support this hypothesis (35, 36). These findings are somewhat discordant with the results of the study by Filbey and colleagues (10), where the G-allele carriers exhibited greater mesocorticolimbic activation than A-allele homozygotes both pre- and post-priming, although the absence of a pre- versus post-priming
