Disruptions to hippocampal adult neurogenesis in rodent models of fetal alcohol spectrum disorders

Abstract

ABSTRACT Exposure of the embryo and fetus to alcohol can lead to abnormal physical, neuroanatomical, and behavioral development, collectively known as Fetal Alcohol Spectrum Disorders (FASDs). This mini-review focuses on the negative impact of prenatal alcohol exposure on hippocampal adult neurogenesis, an important process by which the brain adds new neurons throughout the lifespan, and hippocampal dendritic complexity through the discussion of various mammalian models of FASDs. Alcohol-induced aberrations in the outgrowth, phenotype, and stability of dendrites of neurons in the hippocampus and the prefrontal cortex will also be discussed. Timing of alcohol exposure during development (first trimester vs. third trimester-equivalent) can determine whether cell proliferation or long-term cell survival is impaired. Our work demonstrating that third trimester-equivalent exposure has a more significant impact on cell survival and dendritic morphology than rate of cell proliferation. Understanding the impact of prenatal ethanol exposure on adult neurogenesis is important as altered rates of new cell generation or successful integration of adult-born neurons could contribute to many of the hippocampal-associated deficits in memory and cognitive function observed in patients with FASDs. In addition, this commentary discusses evidence in support of aerobic exercise and environmental complexity (“enrichment”) as potential therapeutic strategies for alcohol-related deficits.