exposure to high doses of alcohol (Rubert, Miñana, Pascual, & Guerri, 2006). Maternal alcohol consumption from E7–E21 in the rat model (25% v/v alcohol) has been shown to reduce proliferation and induce rapid differentiation via down-regulation of Notch pathway factors (Kim et al., 2010). The increase in levels of Ndn may exacerbate these anti-proliferative effects of PAE, as Ndn facilitates cell cycle arrest, acts as a growth suppressor, and has been shown to suppress NPC proliferation in the embryonic neocortex (Minamide, Fujiwara, Hasegawa, & Yoshikawa, 2014). While we were unable to find other studies demonstrating a connection between Ndn and alcohol exposure, it is likely that Ndn is impacted by alcohol. Ndn is an imprinted gene and since alcohol has been demonstrated to deplete methyl donors, lack of DNA methylation due to alcohol exposure may result in increased expression of this particular gene, similar to alcohol's effect on Sox3 methylation (Haycock, 2009; Zhou et al., 2011). Alterations in these genes suggest that PAE results in perturbed cell growth; however, it is possible that the observed increase in expression of Fgf13 and Sox3 could be a compensatory mechanism to shift the emphasis back to self-renewal and stem cell maintenance programs. Sox3,
