Positron Emission Tomography (PET) imaging findings suggest that in alcohol-dependent individuals, D2-dopamine receptor availability in the ventral striatum is negatively associated with alcohol craving (Heinz et al., 2005b). Moreover, lower availability of D2-like receptors in the ventral striatum was associated with greater alcohol craving and greater cue-induced activation of the mPFC and ACC during an fMRI task in alcohol dependent patients (Heinz et al., 2004). PET imaging has implicated the mu-opioid receptors in alcohol craving, such that higher availability of mu-opioid receptors in the ventral striatum and mPFC was positively associated with the degree of craving in alcohol dependent patients (Heinz et al., 2005a). Furthermore, drinking alcohol induces opioid release in the NAc and OFC (Mitchell et al., 2012) and a genetic polymorphism of the mu opioid receptor (OPRM1) gene is associated with stronger dopamine release in the ventral striatum following alcohol consumption (Ramchandani et al., 2011). These studies implicate both endogenous opioids and dopamine in the ventral striatum with the expression of alcohol craving and alcohol “high”, which are thought to subserve goal-directed drinking. Thus, variation in striatal opioid levels may moderate the efficiency of fronto-striatal control over craving and genetic markers subserving opioidergic activity warrant examination.
