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, including the corticostriatal synapses examined by Meinhardt et al. (2013). Indeed, increased extracellular NAc glutamate, induced by chronic ethanol or glutamate reuptake inhibition, promoted ethanol consumption in mice (Griffin et al., 2014). Based on this line of work, glutamate uptake has been targeted to treat AUD (Rao et al., 2015).
