Alcohol deprivation effect (ADE), i.e. the transient increase in alcohol intake that takes place in laboratory animals after a period of alcohol deprivation, has been proposed to model alcohol relapses in alcoholics. The present study investigated the effect of the GABA(B) receptor agonist, baclofen, on the development of ADE in selectively bred Sardinian alcohol-preferring (sP) rats. Acute administration of non-sedative doses of baclofen (0, 1, 1.7 and 3 mg/kg, i.p.) resulted in the complete suppression of the extra-amount of alcohol consumed during the first hour of re-access to alcohol after 7 days of deprivation. These results implicate the GABA(B) receptor in the neural substrate mediating ADE and suggest that baclofen may possess anti-relapse properties.