Developmentalexposure to low lead (Pb) doses induces elevated voluntary ethanol intake inrats, an effect that we attribute to central acetaldehyde (ACD) accumulation,which is considered reinforcing. Furthermore, this metabolite reacts with dopamine(DA) to form salsolinol (SAL) inducing DA release. Based on previous evidenceof ACD involvement in the reinforcing effects of ethanol in Pb-exposed animals,we here postulate that SAL may mediate these differential effects. To this end,SAL (10 mg/kg i.p.) or vehicle was administered at the end of the voluntaryethanol intake test (2-10% for 28 days) to register voluntary ethanolconsumption and subsequent locomotor activity. In addition, a group of animals thatwere not submitted to the ethanol protocol was included as control. The resultsindicate that SAL administration failed to modify ethanol consumption, but evidenceda statistically significant increase in locomotor activity in Pb exposed animalsthat consumed ethanol and were injected with SAL, indicating a heightenedresponse to the stimulant effects of ethanol. These results provide furthersupport to the hypothesis that ACD (and thereby SAL) is involved in theheightened ethanol-related effects observed in the Pb-exposed animals.