mGlu2 and mGlu3 expression levels were significantly lower in the AcbSh and CeA of adult ethanol-naive P versus NP rats.209,211 As discussed earlier, Zhou and coworkers202 reported a stop-codon polymorphism of mGlu2 in P, but not present in NP rats that appear to predispose them to high ethanol consumption. And, multiple studies134,135,141,143,145 have shown that mGlu2/3 agonists, presumably acting at the presynaptic autoreceptor, block ethanol-self-administration, -seeking, and -relapse behavior in P rats. Noteworthy is the fact that mGlu4, mGlu5, mGlu7, and mGlu8 (all are involved with inhibitory activity, generally at the presynaptic terminal) are also significantly lower in the AcbSh of P versus NP rats. Gene expression for only one mGluR, mGlu1, was ~1.4-fold higher in the AcbSh of P versus NP rats, which is a finding consistent with prior results from inbred C57BL/6J versus DBA2/J mice.86 Regarding the effects of ethanol, operant ethanol self-administration by adult P rats significantly reduced mGlu1 (~20% decrease) expression levels in the AcbSh, relative to ethanol-naive P rats.214 Given mGlu1’s basal elevation, relative to NP rats, it is possible that ethanol self-administration could reverse
