Finally, the incentive sensitization theory proposes that heavy prolonged exposure to alcohol results in both increased salience of drug cues as well as neuroadaptations that sensitize brain circuits in regions specifically involved in motivation or ‘wanting’ of the drug, but not necessarily hedonic ‘liking’ of the drug (Robinson and Berridge, 1993). Findings from previous studies have suggested that individuals with a low subjective response to alcohol display increased neural responses reflecting enhanced incentive value of alcohol cues (Bartholow et al., 2007, 2010) as well as automatic approach tendencies to alcohol cues reflecting greater ‘wanting’ (Fleming and Bartholow, 2014). This increased salience is thought to result from neuroadaptations that sensitize the mesolimbic dopamine pathway to specific drug effects and related stimuli. Evidence has shown that acute alcohol administration acts on μ-opioid receptors to produce the hedonic ‘liking’ effects and subsequently modulate activity of dopaminergic neurons that produce the ‘wanting’ effects. However, it is unclear to what extent these OPRM1 variants (rs3778150 and rs1799971) might influence incentive sensitization processes and subsequent risk for problematic alcohol use, given that the current study was
