were significantly and inversely related to ethanol consumption, with decreases in mGlu2 and mGlu2 receptor expression associated with significant increases in ethanol-drinking behavior.202 Similarly, mGlu2 knockout mice display significantly greater ethanol consumption and preference than their wild-type counterparts.202 As mGlu2 receptors function as autoreceptors, the results indicate an inverse relationship between mGlu2 gene/protein expression and ethanol intake, which is consistent with the aforementioned hypothesis that excessive drinking phenotypes are associated with a hyperglutamatergic state.
