Acute ethanol treatment in rats elicits a selective increase in dihydroxyphenylacetic acid (DOPAC) content in striatum. In contrast, striatal DOPAC concentration does not differ from normal values after chronic ethanol treatment. Chronic administration of ethanol however causes a selective increase of specific [3H]spiroperidol binding and met‐enkephalin content in the striatum. Kinetic analysis of [3H]spiroperidol binding data shows that after chronic ethanol treatment there is a significant increase in the affinity constant rather than in the number of binding sites for the ligand. Our results support the hypothesis that dopaminergic mechanisms at both pre‐ and postsynaptic level may be involved in the mediation of some of the central effects observed after ethanol consumption.