The acute ethanol-induced increase in dopamine neuron firing is associated with increased NAc dopamine levels in rodents (Ericson et al., 1998; Yoshimoto et al., 1992) and humans (Aalto et al., 2015; Boileau et al., 2003) (Figure 2E). Interestingly, active and passive ethanol administration produces similar increases in NAc dopamine levels (Bassareo et al., 2017) that may be dependent on taurine (Ericson et al., 2011), GlyRs (Adermark et al., 2011a), and opiate receptors (Benjamin et al., 1993; Zapata and Shippenberg, 2006) (Figure 2F). In contrast, high concentrations of ethanol dampen dopamine release from terminals measured with fast-scan cyclic voltammetry in the striatum (Budygin et al., 2001; Schilaty et al., 2014). These seemingly contradictory effects of ethanol on the striatal dopamine depend on the ethanol dose, with lower doses increasing dopamine via actions in midbrain and higher doses inhibiting release. Chronic ethanol 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
