IBCN   20355
INSTITUTO DE BIOLOGIA CELULAR Y NEUROCIENCIA "PROFESOR EDUARDO DE ROBERTIS"
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
PRENATAL ETHANOL EXPOSURE: EFFECTS ON POSTMITOTIC NEURONAL MIGRATION IN THE FETAL CEREBARL CORTEX
Autor/es:
ARONNE MP, GUADAGNOLIN T, EVRARD SG, BRUSCO A
Lugar:
SAN DIEGO
Reunión:
Congreso; 40º ANNUAL MEETING; 2010
Institución organizadora:
SOCIETY FOR NEUROSCIENCE
Resumen:
Prenatal ethanol exposure (PEE) induces morphofunctional alterations in the developing Central Nervous System (CNS). The relationship between radial glia cells (RGC) and migrating neuroblasts is crucial for the establishment of normally 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 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 EtOH-induced alterations in the fetal cerebral cortex on gestational days (G) 12, G14, G16 and G18. 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. In the present work we observed a marked delay in the migration process of postmitotic neuroblasts and alterations in the expression of the transcription factor Pax6 in the developing cerebral cortex of treated fetuses. Our data suggest that PEE strongly affects neuronal migration and corticogenesis. These morphological alterations could be involved in the patophysiology of neurodevelopment disorders observed in the children of alcoholic mothers affected by the fetal alcohol syndrome