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

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 minireview 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 trimesterequivalent exposure has a more significant impact on cell survival and dendritic morphology than rate of cell proliferation. Understanding th)