is another growth factor important for cell proliferation, dendritic outgrowth, and synapse formation, particularly in the adult brain. Numerous studies have demonstrated that development alcohol exposure causes long-term changes to functional and anatomical measures linked to BDNF signaling, including long-term potentiation (Puglia and Valenzuela, 2010), adult neurogenesis (Boehme et al., 2011; Gil-Mohapel et al., 2010; Hamilton et al., 2011; Klintsova et al., 2007), and dendritic morphology (Berman et al., 1996; Boschen et al., 2016; Hamilton et al., 2015; Hamilton et al., 2010; Redila and Christie, 2006; Whitcher and Klintsova, 2008). Studies have demonstrated that Bdnf gene expression is altered following developmental alcohol exposure in a timing and region-specific manner (Caldwell et al., 2008; Feng et al., 2005; Heaton et al., 2000; Heaton et al., 2003), though the diverse models and methods of analysis used in these studies makes it difficult to draw definitive conclusions. Epigenetic modification of Bdnf has not been well studied in alcohol exposure models, despite being a significant target of interest in prenatal stress research. Bdnf exon I hypomethylation was reported 24 h following PD4–9 alcohol exposure in the male rat hippocampus; this reduction in methylation was correlated with increased exon I-driven Bdnf gene expression (Boschen et
