Although much research has focused on neuronal populations in alcohol use, glial cells comprise a vital component in the proper functioning of the nervous system and regulate synaptic plasticity (Dallerac, Chever, & Rouach, 2013; Oliet, Piet, & Poulain, 2001). The role of glia in neuroinflammatory processes that regulate neuronal function is well recognized in the context of drug phenotypes (Miguel-Hidalgo, 2009). Studies have shown that ethanol induces the transcription factor, NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) which induces a host of pro-inflammatory molecules that may be epigenetically regulated (Crews, Zou, & Qin, 2011; Ponomarev et al., 2012). Cocaine exposure has also been shown to induce NF-κB expression in the NAc where it regulates dendritic spines and sensitization (Russo et al., 2009). NF-κB and related transcription factors integrate various signals and regulate, via epigenetic and chromatin-remodeling pathways, corresponding targets to bring about distinct cellular outcomes (Meffert, Chang, Wiltgen, Fanselow, & Baltimore, 2003; Natoli, Saccani, Bosisio, & Marazzi, 2005). Neuroinflammation induced following chronic ethanol use and withdrawal was shown to occur via Toll-like receptor signaling (TLR4) and activation of the
