Perinatal lead (Pb)-exposureinduces higher ethanol intake in adolescent animals compared to non-exposedcontrols, likely due to brain ACD accumulation which is considered reinforcing. We here sought to determine whether ALDHexpression in limbic regions (prefrontal cortex -PfC, caudate-putamen ?CP, andnucleus accumbens -NAc) is modified by developmental Pb exposure. Thirty five-day old male Wistar rats were offered with ethanol (2-10%v/v) or water during 28 days. Twoadditional groups were included as controls: 35 and 63 day-old animals thathave not consumed ethanol (non-ethanol groups). At the end of the study all the animals were perfused,the brain fixed, and immunohistochemistry performed forALDH abundance. The results evidence that ALDH expression was notaffected by perinatal Pb exposure, given that both control and Pb-exposed adolescentanimals showed comparable cell counts in the three regions analyzed. However,ethanol intake induced a dramatic reduction in the Pb-exposed group?s ALDHpositive cells in all three regions when they were assessed at the end of the ethanolintake test. This effect was blunted in the NAc and CP from animals notsubmitted to the ethanol consumption protocol, while the PfC data showed araise in cell count number in the Pb-exposed rats that deserves furtherconsideration. The results indicate lower ALDH expression in key brain regionsthat could led to brain ACD accumulation and consequent higher ethanol intakein Pb-exposed animals.