exposure produces adaptations in dopamine release, and the opioid system may play a role (reviewed in Barbaccia et al., 1980). A nonspecific opioid receptor antagonist blocks dopamine release induced by ethanol drinking in the NAc (Gonzales and Weiss, 1998). Recent work has also shown that the ethanol-induced dopamine increase switches to a decrease after short-term withdrawal, which could be associated with a supersensitivity of kappa opiate receptors (Karkhanis et al., 2016; Rose et al., 2016; Siciliano et al., 2015) (Figure 3D). Interestingly, decreased availability of striatal D2 dopamine receptors is associated with AUD (Volkow et al., 2002; Volkow et al., 2017) (Figure 3D), indicating less dopamine responsiveness after short-term withdrawal from chronic ethanol exposure. Hirth et al. (2016), however, found that while dopamine levels were decreased during acute ethanol withdrawal, protracted withdrawal was accompanied by increased dopamine in rodents. Thus, while the overall trend is a decrease in dopaminergic transmission after chronic ethanol and withdrawal, this may depend on the withdrawal duration.
