Chunk #20 — 3. Biological co-expression networks: Transcriptional regulation in alcohol use disorder — 3.1: Epigenetic modifications in the human alcoholic brain
In addition to altered DNA methylation, histone modifications are also prevalent in human alcoholic brain (Ponomarev et al., 2012). Moreover, these changes are observed in other species. For example, binge consumption of alcohol in humans and daily operant alcohol self-administration in rats both increased HDAC expression in peripheral blood (Lopez-Moreno et al., 2015). In rodent models, several studies reported ethanol-induced epigenetic alterations in H3 acetylation and HDAC expression (Pandey et al., 2008; Pascual et al., 2012; Starkman et al., 2012; Warnault et al., 2013). Ethanol-induced changes in HDAC expression have also been observed in neuronal cell culture models (Agudelo et al., 2011; Agudelo et al., 2012). HDAC inhibitors are effective in countering ethanol-induced behaviors and epigenetic changes in HDAC. For example, trichostatin A (TSA) treatment reversed ethanol-induced tolerance, drinking, and anxiety by inhibiting HDAC activity in the amygdala of rats (Alaux-Cantin et al., 2013; Sakharkar et al., 2014). Treatment with the HDAC inhibitor sodium butyrate blocked both the acquisition and the expression of ethanol-induced behavioral sensitization in mice (Legastelois et al., 2013). Furthermore, systemic treatment of HDAC class I and
