Many of the genes that had lower expression levels in the alcohol than water group could result in altered transcription (Chd7, Klf3, Mga, Mtf1, Sp1; Kim and Layman 2011; Moore et al., 2011; Hurlin et al., 1999; Giedroc et al., 2001; Lomberk and Urrutia 2005), and reduced response to oxidative (Angptl4; Zhu et al., 2012) or other cellular (C1s, Cdkn1a, Limd1; Schumaker et al., 1986; Mergenthaler et al., 2013; Foxler et al., 2012) stresses. These results suggest that adolescent binge-like alcohol drinking may have reduced the capabilities of many of the neurons and glia in the Acb-sh and CeA to adequately regulate the levels of reactive oxygen species. Interestingly, Limd1 was identified as a high alcohol consumption candidate gene in a meta-analysis study with mice (Mulligan et al., 2006).
