CONSEQUENCES OF PRENATAL ETHANOL EXPOSURE ON THE POSTMITOTIC NEURONAL MIGRATION IN THE FETAL CEREBRAL CORTEX

ARONNE MP, GUADAGNOLI T, EVRARD SG, BRUSCO HA.

Rio de Janeiro

Congreso; 13th International Symposium on Tobacco Treatment 9th International Symposium on Alcohol and Other Drugs / 1st Latin American Symposium of the International Drug Abuse Research Society; 2010

Drug Abuse Research Society

Prenatal Ethanol Exposure (PEE) induces morphofunctional alterations in the developing Central Nervous System (CNS). The close relationship between developing glia and neurons regulates both neurogenesis as the normal establishment of nuclei, tracts and stratification of laminated structures. Neuronal migration is a key process in the developing and adult brain. The cerebral cortex is formed by the orderly migration and subsequent differentiation of neuronal precursors that were generated from neuroepithelial cells in the proliferative ventricular zone. The transcription factor Pax6 is expressed in these cells from the initial stages of CNS development and in neurogenic niches. Pax6 plays pivotal roles in various aspects of the corticogenesis and in various developmental processes, such as neuronal migration. In this study, one month before mating, and during pregnancy and lactation, female Wistar rats were fed a liquid diet with 5.9% (w/w) ethanol (EtOH). We analyzed the alterations induced by the EtOH in the fetal cerebral cortex on the gestational day (G) 12, G14, G16, G18 and at the third postnatal day (P3). Under these experimental conditions, we studied at each stage the migratory pattern of the postmitotic neuroblasts through the cerebral cortex and the expression pattern of Pax6, involved on the continual regulation of cell surface properties responsible for both cellular identity and radial migration, defects of which cause regional cell sorting and abnormalities of migration in the treatment with EtOH. At the present work we observed a marked delay in the postmitotic neuroblasts migration process and alterations in the expression of the transcription factor Pax6 in the developing cerebral cortex of treated fetuses.