CONICET | Buscador de Institutos y Recursos Humanos

Recent research suggests that ethanol administration in developing rat can produce alterations in the normal brain synaptogenesis and apoptotic mechanisms. During the period of synaptogenesis (postnatal days 1-15 in rats) has been reported that ethanol cause apoptotic neurodegeneration in some brain structures as the hippocampus. The main goal of this study is to determine if ethanol increases apoptosis during this developmental period in the Central Extended Amygdala (AMExCe), an important structure implicated in emotional and social behaviours. Methods: 7 and 15 day-old male Wistar rats were used. Treated rats: administrated with Ethanol 20% sc, 2.5g/Kg at 0hs and 2.5g/Kg two hours after. Control rats receive saline. All animals were fixed with paraformaldehyde 4% in Borato Buffer. At both ages brains were studied at survival times of 2, 4, 6, 8, 12 and 24 hours post-administration. The Amino-Cupro-Silver technique was used to reveal neurodegeneration. Cells were counted, in 60ìm sections, with the KS Lite program. ANOVA was used for statistics with a p<. 05 of significance limit. RESULTS: In the structures that integrates the AMExCE (Intersticial Nucleus of Stria Terminalis and Central Amygdaloid Nucleus) there were significant differences between ethanol and control treated rats (p<.001) in all survivals periods. Significant amounts of dead neurons respect to controls were detected at 2 hours after ethanol, increasing at 4, 6, 8 and 12 hours reaching peak values at 24 hours, showing the vulnerability of AMExCE to the drug. The present data indicates the vulnerability of the AMExCE neurons to ethanol toxicity, as demonstrated by the increase in apoptotic neuronal death, in the early postnatal period of brain development. POSTER- AREA: DESARROLLO