Repeated exposure to ethanol (often accompanied by several withdrawal/forced abstinence periods) alters several aspects of dopaminergic function in SNc and dorsal striatum (Rothblat, Rubin et al. 2001). It should be noted, however, that most of the studies examining these effects did not differentiate between different dorsal striatal subregions. Tissue levels of DA and DA metabolites are decreased in dorsal striatum, cortex and SN following chronic alcohol administration (Fadda, Argiolas et al. 1980, Kaneyuki, Morimasa et al. 1991), and a similar effect has also been observed following ethanol injections (Fadda, Mosca et al. 1989). Stimulated release of DA in DS is also reduced following chronic ethanol exposure in adolescent rat (Palm and Nylander 2014), and following drinking in adult monkeys (Siciliano, Calipari et al. 2015), and mixed effects have been seen in other assays of release (Hunt, Majchrowicz et al. 1979). Increased inhibition of DA release by kappa opiate receptors was also observed in monkey caudate following chronic ethanol drinking (Siciliano, Calipari et al. 2015). Increases in ligand binding to dopamine transporters and increased DA uptake in DS have also been
