Chronic prenatal ethanol exposure does not affect the expression of selected genes in rat brain development.

To investigate possible mechanisms contributing to the teratogenic effects of ethanol on the nervous system, we examined the effects of in utero exposure to ethanol on gene expression in the postnatal brain. Pregnant rats were exposed to ethanol by constant inhalation of ethanol vapor during gestational days 8-21, generating a mean blood alcohol level of approximately 150 mg/100 ml during the last week of gestation. Particular care was given to ensure proper nutrition and weight gain in both control and EtOH-treated groups. At different times after birth, the brains of pups from ethanol-treated dams and from a parallel series of untreated dams were dissected into major regions. Cytoplasmic RNA was assayed for different mRNAs encoding proteins representative of both glial and neuronal cell types, by Northern blot and solution hybridization. In situ hybridization was performed with T alpha-1 tubulin and PLP. There were no significant differences between pups from ethanol-treated and control dams in the amount of mRNAs encoding the myelin protein proteolipid protein (PLP), the astrocyte glial fibrillary acidic protein (GFAP), the neurally enriched T alpha-1 isotype of alpha-tubulin, the nerve terminal components synaptophysin p38 and SNAP 25. The mRNA encoding the alpha 1-subunit of the receptor for gamma-amino butyric acid (GABA) was slightly decreased in expression in the hindbrain but not cortex of pups from EtOH-treated dams. These results suggest that, when weight gain is controlled, chronic exposure of rats to ethanol during the last 2 weeks of gestation has little influence on the postnatal expression of these cell type specific genes.