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 These observations are paralleled by intracranial self stimulation (ICSS) studies showing that ethanol-withdrawn rats are capable of maintaining the ICSS behavior provided that the stimulus current intensity is increased (Schulteis et al., 1995). This important observation strongly indicates that the neural substrate responsible for maintaining the ICSS behavior is hyperpolarized, or more refractory, in the alcohol-dependent subject as compared with its control. Since the neural substrate of ICSS involves DA axons (Yeomans, 1989; Yeomans et al., 1993) near the stimulating electrode, the results are complementary to those reported above and well support a deficitary function of DA neurons. In addition, the perseverance of the reduction in DA activity (beyond resolution of somatic signs of withdrawal) has also been documented in morphine-dependent rats (Diana et al., 1999), while a dichotomy between DA function and somatic withdrawal has been observed in cannabinoid–withdrawn rats (Diana et al., 1998). Similarly, conditioned heroin withdrawal decreases reward sensitivity (Kenny et al., 2006) which persists well beyond the initial phase of withdrawal. These findings, observed across different addicting compounds and experimental conditions, suggest that DA hypofunction persists
