Chronic D1-agonist treatment facilitates ethanol reward
It has been hypothesized that interactions between D1-type dopamine receptors and NMDA type glutamate receptors in the nucleus accumbens are involved in behavioral and biochemical manifestations of drug abuse. In the present study, the rewarding effects of intravenous (i.v.) ethanol were assessed after chronic treatment with a D1 agonist and/or ethanol. Operant-trained Sprague Dawley rats were treated with experimenter-administered i.v. saline, ethanol (2.0 g/kg), the D1 agonist, SKF 81297 (0.2 mg/kg) or the co-administration of SKF 81297 and ethanol. After four weeks of treatment, rats were given access to i.v. ethanol (250 mg/kg/inj) during one hour sessions. Animals that had been pre-exposed to the co-administration of ethanol and SKF 81297 or SKF 81297 alone self-administered behaviorally relevant levels of i.v. ethanol (up to 2.5 g/kg), while those that had been treated with saline or ethanol alone did not (<1.0 g/kg). These data suggest that D1 receptor activation is an important component in a neurobiological pathway that engenders rewarding ethanol effects.