seeking after ethanol abstinence in Long Evans rats (Lebourgeois et al., 2018). Unlike ceftriaxone, N-acetylcysteine does not affect cue-primed reinstatement of ethanol seeking in Sprague-Dawley rats, suggesting mechanisms other than modulating glutamate uptake contribute to these behaviors (Weiland et al., 2015). Another drug that increases GLT-1 expression, clavulanic acid, has recently been shown to decrease ethanol drinking in rats (Hakami and Sari, 2017). Administration of anti-inflammatory mesenchymal stem cells (MSC) decreases ethanol consumption and relapse drinking, possibly through upregulation of GLT-1 expression (Ezquer et al., 2018). MSC administration also normalizes ethanol-induced changes in astrocyte reactivity, oxidative stress, and inflammatory marker expression. Thus, astrocyte glutamate homeostasis is important in regulating ethanol drinking, and inflammatory environments can hinder the functionality and expression of proteins required for proper homeostasis. Potential roles for glial glutamate transporters in AUD are reviewed in more detail in (Ayers-Ringler et al., 2016).
