Astrocytes also regulate neuronal activity through gliotransmission (i.e., the astrocytic release of neuromodulators) elicited by increases in intracellular Ca2+ levels (Martín-Fernández et al., 2017; Oliveira et al., 2015; Theodosis et al., 2008; Yang et al., 2015). In cultured astrocytes, ethanol induces Ca2+ transients and gliotransmission, causing release of transmitters such as glutamate, glutamine, and taurine (Kimelberg et al., 1993; Salazar et al., 2008), as well as inflammatory ROS (González et al., 2007). Ethanol also affects downstream neurotransmitter-mediated responses in astrocytes, such as stimulating serotonin-induced inositol metabolism and suppressing muscarinic receptor-mediated Ca2+ responses in astrocytes (Catlin et al., 2000; Simonsson et al., 1989). Ethanol thus has several mechanisms through which it alters astrocyte-neuronal signaling. Transcriptome sequencing of cortical astrocytes isolated from mice following chronic ethanol consumption shows ethanol-induced transcriptome changes in Ca2+ signaling, further implicating this mechanism in ethanol responses (Erickson et al., 2018). Gap junction hemi-channels such as connexin 43, which help propagate Ca2+ signals in astrocytes, are also differentially expressed by ethanol exposure (Adermark and Lovinger, 2006; Adermark et al., 2004; Miguel-Hidalgo et al., 2014). A few studies have
