Consequences of SAL administration in voluntary ethanol consumption and subsequent locomotor activity in perinatally lead-exposed rats

ALBRECHT P.A; DEZA-PONZIO R; MATTALLONI M.S; ; CANCELA L.M; VIRGOLINI M.B

Mar del Plata

Congreso; XXX Congreso Anual de la Sociedad Argentina de Investigación en Neurociencias; 2015

Sociedad Argentina de Investigación en Neurociencias

Developmental exposure to low lead (Pb) doses induces elevated voluntary ethanol intake in rats, 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 evidence of 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 voluntary ethanol intake test (2-10% for 28 days) to register voluntary ethanol consumption and subsequent locomotor activity. In addition, a group of animals that were not submitted to the ethanol protocol was included as control. The results indicate that SAL administration failed to modify ethanol consumption, but evidenced a statistically significant increase in locomotor activity in Pb exposed animals that consumed ethanol and were injected with SAL, indicating a heightened response to the stimulant effects of ethanol. These results provide further support to the hypothesis that ACD (and thereby SAL) is involved in the heightened ethanol-related effects observed in the Pb-exposed animals.