Acute response of the fetal telencephalon to short-term maternal exposure to ethanol in the rat.

Pregnant rats were exposed to either ethanol (total dose 18 g/kg) on gestational days 14 and 15 or whole-body ionizing radiation (0.5 Gy) on gestational day 15. On gestational day 16, 24 h following the last dose of ethanol or exposure to ionizing radiation, the developing cerebral cortex of the fetus was examined histologically. Ionizing radiation caused extensive cell death within the fetal cerebral cortex whereas ethanol caused more subtle morphological changes such as cortical thinning and petechial intraventricular hemorrhages. These findings suggest that ethanol, unlike ionizing radiation, acts by some mechanism other than cell death to cause cortical thinning and cortical malformations. The pathogenesis of ethanol-induced cortical dysgenesis may include fetal hypoxia and inhibition of neuroblast proliferation within the developing cerebral cortex.