Chronic ethanol exposure can affect NMDARs (Abrahao et al., 2013; den Hartog et al., 2017; Hendricson et al., 2007), kainate receptors (Carta et al., 2003; Läck et al., 2009), AMPA receptors (AMPARs) (Läck et al., 2007), and metabotropic glutamate receptors (mGluRs) (Ding et al., 2016; Mihov and Hasler, 2016). These ethanol effects in specific brain regions have been linked to different ethanol-related phenotypes. For example, increased glutamatergic transmission in the BLA induced by chronic ethanol is associated with withdrawal anxiety-like behavior (Christian et al., 2013; Läck et al., 2007) (Figure 3H). In addition, selective deletion of the GluN2B NMDAR subunit in cortical interneurons reduces ethanol seeking (Radke et al., 2017a, 2017b) (Figure 3I). Analysis of the role of glutamate and glutamate receptors in ethanol-related behaviors should be extended to additional synapses and brain regions. Chronic ethanol exposure elevates extracellular glutamate levels in several brain regions, inducing a “hyperglutamatergic” state thought to contribute to AUDs (Gass and Olive, 2008; Spanagel, 2009). For example, this increased glutamatergic drive may lead to excessive activation at key synapses in circuits involved in ethanol seeking,
