Fetal Alcohol Exposure and Hippocampal Dysfunction in the Vervet Monkey

Exposure to ethanol in utero is recognized as a leading cause of preventable developmental disorder. Children with fetal alcohol syndrome disorders (FASD) display behavioral and intellectual impairments that strongly implicate the hippocampus, an area essential for learning and memory. Small animal models indicate the third trimester equivalent as a critical period for hippocampal damage. We have developed a non-human primate model where dams voluntarily and naturally consume alcohol in a minimally stress environment. We have found even low-moderate fetal alcohol exposure (FAE) leads to reduced neuronal populations in the hippocampus, along with reduced immature neuronal population and stem cell activity. This model provides a platform in which to test potential therapeutic interventions to minimize the effects of fetal alcohol exposure.