Alcohol-dependent (in the present context the term “dependent,” when referred to a non-human experimental subject, indicates a condition in which the subject has shown unequivocally a proof of dependency, i.e., somatic signs of withdrawal) rats show a profound reduction of spontaneous firing rate and burst firing of antidromically identified Nucleus accumbens (Nacc)-projecting ventral tegmental area (VTA) DA-containing neurons in rats (Diana et al., 1993) and mice (Bailey et al., 2001) resulting in a concomitant reduction of microdialysate DA in the Nacc (Rossetti et al., 1992; Diana et al., 1993; Barak et al., 2011). Further, the reduced dopaminergic activity outlasts somatic signs of alcohol-withdrawal (Diana et al., 1996, 2003) thereby suggesting a role for DA in the lasting consequences of alcohol dependence while excluding the possibility of a DA role in somatic aspects of withdrawal. Further, original (pre-dependence) DA levels in the Nacc are restored when ethanol is self (Weiss et al., 1996) and/or passively administered (Diana et al., 1993, 1996). These observations are paralleled by intracranial self stimulation (ICSS) studies showing that ethanol-withdrawn rats are capable of maintaining the ICSS
