In rats, the compound BINA, which potentiates the mGluR2 receptor, reduced hyperactivity and brain activation caused by the NMDA antagonist PCP, a model of schizophrenia symptoms. BINA suppressed PCP-induced blood oxygenation level-dependent (BOLD) signals in the prefrontal cortex, caudate-putamen, nucleus accumbens, and mediodorsal thalamus. These findings support mGluR2 as a viable target for schizophrenia treatment.
Nitrous oxide, a gas that blocks NMDA receptors, did not produce a rewarding effect on its own but impaired the acquisition of morphine-induced conditioned place preference and blocked the expression of both cocaine- and morphine-induced conditioned place preference in mice. The effects lasted for four days after exposure. No changes were observed in tests of attention, anxiety, depression, locomotion, or anhedonia, indicating the gas's effects were specific to the conditioned place preference. The findings suggest nitrous oxide may have clinical potential for treating morphine and cocaine addiction.