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 investigated the role of astrocyte Ca2+-related signaling in ethanol-seeking behaviors. Gap junction hemi-channel blockade in the NAc core, which impairs communication between astrocytes, increases ethanol-seeking behavior (Bull et al., 2014). In contrast, activating Ca2+ signaling in NAc core astrocytes in rats using DREADDs reduces motivation to self-administer ethanol after 3 weeks of abstinence (Bull et al., 2014). Another study using DREADDs to stimulate astrocytes in the NAc core to inhibit cocaine seeking shows that Ca2+ activation induces glial glutamate release (Scofield et al., 2015). These findings indicate that ethanol alters astrocyte Ca2+ signaling and intercellular communication, which may regulate addiction-related behaviors via changes in gliotransmission.
