Developmental lead exposure induces opposite effects on ethanol intake and locomotion in response to central vs. systemic cyanamide administration

MATTALLONI MS; DEZA-PONZIO R; ALBRECHT P; CANCELA LM; VIRGOLINI MB

ALCOHOL

ELSEVIER SCIENCE INC

Lugar: Amsterdam; Año: 2017 vol. 58 p. 1 - 1

0741-8329

ead (Pb) is a developmental neurotoxicant that elicits differential responses to drugs of abuse. Particularly, ethanol consumptionhas been demonstrated to be increased as a consequence of environmental Pb exposure, with catalase (CAT)and brain acetaldehyde (ACD, the first metabolite of ethanol) playing a role. The present study sought to interfere withethanol metabolism by inhibiting ALDH2 (mitochondrial aldehyde dehydrogenase) activity in both liver and brain controland Pb-exposed rats as a strategy to accumulate ACD, a substance that plays a major role in the drug´s reinforcingand/or aversive effects.To evaluate the impact on a 2-h chronic voluntary ethanol intake test, developmentally Pb-exposed and control ratswere administered with cyanamide (CY, an ALDH inhibitor) either systemically or intracerebroventricularly (i.c.v.) onthe last 4 sessions of the experiment. Furthermore, on the last session and after locomotor activity was assessed, all animalswere sacrificed to obtain brain