Abstract

The effects of the mixed dopamine D2/D3 agonist, quinpirole and antagonist, raclopride on ethanol consumption were examined within both a limited and a continuous access paradigm. The goals of these studies were to determine if decreases in ethanol intake after administration of the dopaminergic agents were the result of the type of paradigm employed, reductions of DA-mediated reinforcement or rather to non-specific drug effects, such as locomotor suppression. Experiment 1 demonstrated that quinpirole (0.1 mg/kg) failed to alter ethanol intake in rats exposed to a 1hr-limited access period. Raclopride-treated (0.5 mg/kg) rats significantly decreased their ethanol intake but were ataxic for the entire 1-hr limited access period. These results suggested that manipulations of the D2/D3 receptors at the dose tested had non-specific effects on the consumption of ethanol. Experiment 2 assessed whether the effects obtained within a limited access paradigm were comparable to a 22-hr continuous access paradigm. Similar, to Experiment 1, quinpirole (0.1 mg/kg) failed to attenuate ethanol consumption within a continuous access paradigm. Contrary to Experiment 1, raclopride (0.5 mg/kg) significantly increased ethanol intake during the treatment and post-treatment periods. Taken together, the findings of Experiment 1 and 2 demonstrated that the D2/D3 agents employed did not produce reductions in ethanol intake specific to ethanol reinforcement. Further, the raclopride induced increase in ethanol intake in Experiment 2 is contradictory to previous reports that systemic injections of DA antagonists produce reductions in ethanol intake. The results suggested that the D2/D3 receptors are not likely to be the primary mediators of ethanol intake.