Purpose Fetal alcohol syndrome is a devastating condition that causes cell death through many mechanisms. Neurotransmitter receptors, such as glutamate and gamma-aminobutyric acid (GABA) receptors, are altered by alcohol consumption, which may impact brain development. In this work we examined the effects of prenatal alcohol consumption on the fetal guinea pig brain, specifically the cortex and hippocampus. The goal of this work was to evaluate protein expression of ionotropic glutamate receptor subunits NR2A, NR2B, NR1, GLUR1, GLUR2/3, and GLUR6/7 in fetal guinea pigs that were exposed to ethanol in utero.
Methods Timed pregnant Dunkin-Hartley-strain guinea pigs received daily oral administration of one of the following regimens between gestational days (GD) 2 and 65: (1) 4 g ethanol/kg maternal body weight/day (ethanol group), (2) isocaloric sucrose and pair-feeding (sucrose group); or (3) isovolumetric water (water group) with ad libitum access to food and water for all 3 groups. On GD 63-65, dams were euthanized by decapitation under halothane anesthesia and fetuses were removed by cesarean section. The maternal blood ethanol concentration produced by the ethanol regimen was 71 ± 12 mM. Cerebral cortices and hippocampus were analyzed for receptor subunit expression using Western immunoblotting.
Results In the cerebral cortex, there was no significant difference in glutamate receptor subunit expression when comparing ethanol to sucrose-exposed fetuses. In the hippocampus, there was a significant decrease of approximately 30% in NR2B expression in the ethanol group when compared to the sucrose-fed dams.
Conclusions Hippocampal receptor NR2B expression was decreased in fetuses exposed in utero to ethanol with no significant change in cerebral cortex receptor expression. In contrast, previous work showed increased GLUR2/3 and decreased NR2B cerebral cortex receptor expression in adult guinea pigs exposed to ethanol in utero. These results suggest that ethanol produces age-dependent and region-specific decreases in the expression of NR2B. This action of ethanol could have an impact on synaptic plasticity and contribute to cognitive abnormalities.
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