Another critical function of astrocytes is to regulate synaptic glutamate homeostasis. Astrocytes work to clear extrasynaptic levels of glutamate via different glutamate transporters [i.e., glutamate aspartate transporter (GLAST/EAAT1), glutamate transporter 1 (GLT-1/EAAT2), and cysteine glutamate anti-transporter (xCT)] (Verkhratsky et al., 2015). Glutamine synthetase then converts glutamate to glutamine, which is shuttled back to neurons for reconversion to glutamate for excitatory neurotransmission. The glutamate-glutamine cycle is com-promised in neurological disorders (Nakagawa and Kaneko, 2013) and may be a consequence of altered neuroimmune signaling, considering that pro-inflammatory cytokines modulate the expression and function of astrocytic glutamate transporters (Tilleux and Hermans, 2007). Ethanol also regulates glutamate homeostasis. For example, acute ethanol exposure inhibits glutamate uptake (Aschner et al., 2001; Smith and Navratilova, 1999, 2003), and chronic ethanol downregulates the expression of GLT-1 and xCT (Aal-Aaboda et al., 2015; Sari, 2013). Blocking glutamate uptake in astrocytes (using dihydrokainic acid infusion into the lateral ventricle) reduces binge drinking (Smith et al., 2014), and GLAST KO mice show reduced voluntary ethanol consumption and do not exhibit CPP to ethanol (Karlsson et al., 2012). Alcohol-induced changes in
