Silencing brain catalase ex-pression reduces ethanol intake in developmentally-lead-exposed rats

MATTALLONI MS; SALINAS C; ALBRECHT PA; DEZA-PONZIO R; QUINTANILLA, ME; HERRERA-MARSCHITZ M; CANCELA LM; RIVERA-MEZA, M; VIRGOLINI MB

NEUROTOXICOLOGY

ELSEVIER SCIENCE BV

Lugar: Amsterdam; Año: 2019 vol. 70 p. 180 - 180

0161-813X

ead (Pb) is a developmental neurotoxicant. We have demonstrated that perinatally Pb-exposed rats consumemore ethanol than their control counterparts, a response that seems to be mediated by catalase (CAT) andcentrally-formed acetaldehyde, ethanol?s first metabolite with attributed reinforcing effects in the brain. Thepresent study sought to disrupt ethanol intake (2?10% ethanol v/v) in rats exposed to 220 ppm Pb or filteredwater during gestation and lactation. Thus, to block brain CAT expression, a lentiviral vector coding for a shRNAagainst CAT (LV-antiCAT vector) was microinfused in the posterior ventral tegmental area (pVTA) either at theonset or towards the end of a chronic voluntary ethanol consumption test. At the end of the study, rats wereeuthanized and pVTA dissected to measure CAT expression by Western blot. The LV-antiCAT vector administrationnot only reversed, but also prevented the emergence of the elevated ethanol intake reported in theperinatally Pb-exposed animals, cha