Could the Prenatal ethanol exposure be related with the establishment of cortical dysplasia?

ARONNE MP, GUADAGNOLI T, SAEZ TMM, CALTANA L, FONTANET P, EVRARD S, BRUSCO HA.

Chicago, Estados Unidos

Congreso; 39th Annual Meeting Society for Neuroscience; 2009

Society for Neuroscience

Prenatal ethanol exposure (PEE) induces structural disorders 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. This study was conducted to determine RGC temporal vulnerability as a function of exposure to EtOH during brain development. Pregnant Wistar rats, 200-250 g, were fed one month before and during pregnancy and lactation with a liquid diet with 5.9% (w/w) EtOH; control rats were fed for the same time with a liquid diet without EtOH. Fetuses brain  cortex were studied at embryonic days E12, E14, E16 and E18. Cortical expression of Vimentin (VIM, an RGC cytoskeletal marker) and S-100b protein (a neurotrophic factor, cytosolic marker of RGC during embryonic development) decreased in all gestational ages in fetuses obtained from treated dams.  A significative reduction of cerebral cortex thickness were present at E16 and E18 with and a delay in neuroblast (Nestin+) migration beginning at E14, but it was not evident at E12. At birth, offspring of alcoholic mothers showed body weight reduction. Our results suggest that PEE strongly affects RGC resulting in a delay of neuronal migration and in lower thickness of the cerebral cortex. The cortical dysplasia could be involved in the patophysiology of neurodevelopment disorders observed in the children of alcoholic mothers affected by the fetal alcohol syndrome.