The hippocampus plays a role in both episodic memory formation and anxiety-like behavior (Kheirbek et al., 2012). It is one of the main sites for neurogenesis in the brain (Zhou, Borello, Rubenstein, & Pleasure, 2006), and in rodents, neurogenesis occurs in the hippocampus at higher levels during adolescence than in adulthood (He & Crews, 2007). Ethanol is known to decrease neurogenesis in the hippocampus (Geil et al., 2014). The patterns of gene expression observed in this study (Table 3) provide potential mechanistic explanations for ethanol’s deleterious effects. The Wnt/β catenin pathway is necessary for hippocampal neurogenesis (Lie et al., 2005). Wnt signaling rescues β catenin from proteasomal degradation and allows it to move into the nucleus, where it works with co-regulators in the LEF/TCF family to activate the transcription of multiple genes necessary for neurogenesis (Varela-Nallar & Inestrosa, 2013). Many genes within this pathway had reduced expression in the binge-drinking rats, including disheveled (Dvl2), Lrp1 (lipoprotein receptor 1), GSK3β and Tcf4 (Tables 2, 3). Tcf7l2, a member of the T-cell factor/lymphoid enhancer-binding factor family of high mobility group (HMG) box
