mGluR2 has also been implicated in the control of excessive ethanol intake by dampening corticostriatal input. Chronic ethanol exposure reduces mGluR2 expression in infralimbic NAc shell projection neurons (Meinhardt et al., 2013). This down-regulation contributes to a hyperglutamatergic state within the NAc shell. In an ethanol self-administration paradigm, cues associated with ethanol elicit responding that is especially strong in ethanol-dependent rats and involves limbic corticostriatal circuitry (Meinhardt et al., 2013). Increasing mGluR2 expression in infralimbic projections to the NAc shell attenuates this responding to levels seen in non-dependent rats. Thus, mGluR2 appears to provide a feedback brake on mPFC-drive for excessive ethanol seeking. Interestingly, the alcohol-preferring P rat is a functional mGluR2 knockout, and enhanced ethanol intake is observed in both this rat and mGluR2 knockout mice (Zhou et al., 2013). Inputs to the DMS are also altered by chronic ethanol exposure. Excessive ethanol consumption potentiates glutamatergic transmission via a postsynaptic mechanism at the corticostriatal input and involves a presynaptic mechanism at the amygdalostriatal input (Ma et al., 2017). Chronic ethanol consumption strengthens glutamatergic input to D1-, but not D2-,
