In recent reports it has been indicated that acute and chronic ethanol treatments affect the central dopaminergic system. In particular, after acute ethanol administration it has been detected an increase of dopamine (DA) turnover measured as dihydroxyphenylacetic acid (DOPAC) content in rat corpus striatum. In order to verify the correlation between these neuronal events and the metabolism of ethanol, we measured striatal DA activity after different experimental manipulations of liver function. Ethanol metabolic rate has been stimulated by administering phenobarbital sodium, while liver ethanol metabolism was decreased with a subtotal hepatectomy. In these conditions we found a shift to the left of the time curve for DOPAC levels and a significant reduction of the peak of DOPAC increase respectively. In this paper we report that acetaldehyde induces modifications of the striatal DOPAC content, which become significant after a shorter latency period in comparison with the acute ethanol injection. Our data suggest the hypothesis that the neurochemical effects of ethanol may be mediated by the formation of specific metabolic products.