Ethanol (ETOH) administered acutely to castrate male rats caused a decline in pituitary luteinizing hormone (LH) and prolactin (PRL) secretion. This was associated with an elevation in hypothalamic and median eminence stores of dopamine (DA) that was related to the dose of alcohol given. Pituitary stalk transection (PST) resulted in a significant rise in plasma PRL levels compared to sham control animals, which suggests that DA in the hypophysial portal blood exerted an inhibitory influence on pituitary PRL secretion. The DA agonist bromocriptine failed to alter mean plasma LH levels in stalk-transected rats. The ETOH-treated castrated rats showed a significant rise in circulating PRL after injection of the DA receptor antagonist haloperidol metabolite II (HAL), but the administration of the DA receptor agonist R(-)-apomorphine HCL (APO) caused plasma PRL to decline to near undetectable levels. Plasma LH levels remained unchanged in the HAL- and APO-treated rats and were similar to those of sham controls. These results suggest that lactotroph DA receptors were still functional. Thus our previous finding of ETOH-induced reduction on LH secretion may be attributable to an inhibitory effect by DA on the luteinizing hormone-releasing hormone (LHRH) peptidergic neurons rather than a direct inhibition by DA on the pituitary gonadotroph.