Abstract
Alcohol-related neurodevelopmental disorders are contributors to long-term learning disabilities. Using a model for fetal alcohol syndrome (FAS), we have shown that prenatal alcohol exposure results in adult learning deficits of unknown mechanism. In the developing hippocampus, the NMDA receptor subunit NR2B triggers long-term potentiation, fundamental to learning and memory; these are supplemented by less plastic NR2A subunits in the adult. To understand the mechanism of alcohol-induced learning deficits in FAS, we evaluated NR2B and NR2A expression in the embryo and adult.
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