was readily observed in control rats upon systemic injection of mGluR2/mGluR3 agonists, was also absent in the post-dependent rats, consistent with the lack of mGluR2 function as a presynaptic receptor to downregulate glutamate release upon activation. The role of mGluR2 was further demonstrated by restoring the receptor through bilateral injection of a lentiviral vector expressing mGluR2 into infralimbic cortex. Expression of the receptor significantly reduced alcohol seeking in the post-dependent rats during the cue-induced reinstatement tests.
