rats, peripheral administration of the mGlu2/3 agonist LY379268 significantly reduced extracellular glutamate in the AcbSh of control but not ethanol-dependent rats, suggesting a downregulation of mGlu2/3 function; (5) ethanol-dependent rats displayed greater relapse (almost twice as many responses) and progressive ratio than controls; (6) lentivial knockdown of mGlu2 in the infralimbic mPFC significantly attenuated cue-induced reinstatement of responding in ethanol-dependent but not nondependent rats; (7) mGlu2 knockdown rats did not differ from control rats in operant relapse responding, operant responding for sweetened condensed milk, or locomotor activity in an open-field test; and (8) a RT-qPCR analysis of postmortem ACC samples revealed that alcoholics had significantly less mGlu2 mRNA than their respective controls. An early postmortem study revealed that individuals who had abused nicotine, but not alcohol, displayed greater expression of Slc17a6 and Slc17a7 vesicular glutamate transporters in the VTA.201 However, in individuals who abused both nicotine and alcohol, these increases in Slc17a6 and Slc17a7 were significantly reduced.201
