The posterior ventral tegmental area (VTA) is a neuroanatomical substrate mediating the reinforcing effects of ethanol in rats. Repeated alcohol deprivations produce robust ethanol intakes of alcohol-preferring (P) rats during relapse and increase the reinforcing effects of oral alcohol self-administration. The objective of this study was to test the hypothesis that alcohol drinking and repeated alcohol deprivations will increase the reinforcing effects of ethanol within the posterior VTA of P rats. Groups of female P rats were used (alcohol-naive, continuous access, and repeatedly deprived). Each rat was implanted with a guide cannula aimed at the posterior VTA. Depression of the active lever produced the infusion of 100 nl of artificial cerebrospinal fluid (CSF) or ethanol (25-300 mg%). Each rat was given only one ethanol concentration during the 4-h sessions conducted every other day. Compared with the infusions of artificial CSF, the alcohol-naive group reliably self-infused 75 and 150 mg% ethanol, but not the lower or higher concentrations. On the other hand, the continuous access group had significantly higher self-infusions of 50, 75, 150, and 300 mg% ethanol compared with artificial CSF infusions. The repeatedly deprived group also self-infused significantly more of 50, 75, 150, and 300 mg% ethanol than artificial CSF; moreover, the number of infusions for all four concentrations was higher in the repeatedly deprived versus the continuous access group. Chronic alcohol drinking by P rats increased the reinforcing effects of ethanol within the posterior VTA, and repeated alcohol deprivations produced a further increase in these reinforcing effects of ethanol.The alcohol-preferring (P) line of rats demonstrates a robust alcohol deprivation effect (ADE) under continuous 24-h access (Rodd-Henricks et al., 2000c) and limited access operant conditions. The ADE is defined as a temporary increase in the intake of or preference for ethanol after a period of deprivation (Sinclair, 1972(Sinclair, , 1973. With repeated deprivations, the magnitude and duration of the ADE increase in the P line of rats (Rodd-Henricks et al., 2001;. The neural mechanisms underlying the expression of the ADE are not known.The ventral tegmental area (VTA) dopamine (DA) system seems to have an important role in mediating the actions of ethanol. Electrophysiological studies demonstrated that ethanol administration increased the firing rate of VTA DA neurons in vivo (Gessa et al., 1985) and in vitro after bath application (Brodie et al., 1990(Brodie et al., , 1995. Microdialysis experiments indicated that oral operant self-administration of ethanol increased DA release in the nucleus accumbens (Weiss et al., 1993(Weiss et al., , 1996Melendez et al., 2002). In addition, microinjection of a D 2,3 agonist into the VTA-reduced ethanol intake of P (Nowak et al., 2000) and Long-Evans (Hodge et al., 1993) rats. Injection of a D 2,3 agonist into the VTA has been shown to reduce DA neuronal activity, presumably through its action at D 2 auto...
