Alcohol, like most drugs of abuse, has been shown to profoundly increase dopamine release in the nucleus accumbens of rodents (Tomkins & Sellers, 2001). Yet, human PET studies exploring dopamine signaling in AUD are contradictory. For example, one study reported that intravenous infusions of alcohol caused a significant increase in dopamine (measured by competitive D2/D3 receptor binding via [11C]raclopride) in the right ventral striatum in non-treatment seeking alcoholics, but not in social drinkers (Yoder et al., 2016). By contrast, an alcohol-induced rise in ventral striatal and caudate extracellular dopamine was associated with pleasurable effects of alcohol in non-alcoholics (Aalto et al., 2015). Such differences may be accounted for by genetic polymorphisms: striatal dopamine levels are high in social drinkers who carry the A118G gene variant of the μ opioid receptor. Individuals with this point-mutation display risky alcohol consumption and are more likely to develop AUD (Ramchandani et al., 2011).
