Prenatal Brain Malformations following Acute Ethanol Exposure in the Rat


  • Supported by research grants NS16694 and ES07079 from NIH.

Reprint requests: Stata Norton, Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, Kansas City, KS 66103.


Morphology of the cerebral cortex was studied in fetuses on gestational Day 21 following oral administration of several doses of ethanol (for total doses of 10,15, or 18 g/kg) to pregnant rats on gestational Days 14 and 15, a critical period for the development of the cerebral cortex. All doses of ethanol were associated with a reduction in maternal weight gain, fetal body weight, and placental weight. Only the high dose of ethanol (total dose 18 g/kg) caused significant fetal cortical thinning. Acute exposure of pregnant rats to ethanol produced dose-dependent malformations of the cerebral cortex and hippocampus in fetuses. On gestational Day 21, the 18 g/kg group contained fetuses with severely disorganized cortical architecture, heterotopias of the cerebral cortex, pia and choroid plexus, and status verrucosus deformis. Fetuses from the 10 g/kg group had less severe malformations, such as disorganization of layers of cortical neurons and dentate granule cells while fetuses from the 15 g/kg group had a mixture of severe and minor malformations. This study demonstrates that acute ethanol exposure during a critical period of development in rats can result in brain malformations similar to those reported in human fetuses and neonates from alcoholic mothers.