Results from several studies investigating long-lasting outcomes after prenatal alcohol exposure point to aberrant fetal programming, particularly in the development of the brain, as a mechanism for alcohol's effects (Kleiber, Mantha, Stringer, & Singh, 2013; Zhou, 2012). However, to date, embryonic neurogenesis has not been fully explored in vivo. Cell culture models used for investigating the effects of alcohol during development, while elucidating important findings for the field, lack the ability to recapitulate gestational alcohol exposure. Investigating the pathogenesis of fetal alcohol syndrome requires modeling the phenotype of the disease in the closest approximation possible, which includes the method of alcohol exposure; however, the use of cell culture does allow for more flexible and direct characterization of distinct activities specifically within proliferating neural progenitor systems that are difficult to isolate in vivo. Thus, PAE followed by ex vivo culture is a more physiologically relevant model of alcohol exposure, which allows for assessment of embryonic neurogenesis on particular cellular phenotypes. While acute in vivo alcohol exposure and subsequent gene expression analysis has been performed in either whole embryo or whole brain
