MGlu₁-mediated restoration of prefrontal cortex inhibitory signaling reverses social and cognitive deficits in an NMDA hypofunction model in mice.

ABSTRACT: Extensive evidence supports the hypothesis that deficits in inhibitory GABA transmission in the prefrontal cortex (PFC) may drive pathophysiological changes underlying symptoms of schizophrenia that are not currently treated by available medications, including cognitive and social impairments. Recently, the mGlu₁ subtype of metabotropic glutamate (mGlu) receptor has been implicated as a novel target to restore GABAergic transmission in the PFC. A recent study reported that activation of mGlu₁ increases inhibitory transmission in the PFC through excitation of somatostatin-expressing GABAergic interneurons, implicating mGlu₁ PAMs as a potential treatment strategy for schizophrenia. Here, we leveraged positive allosteric modulators (PAMs) of mGlu₁ t

SUBMITTER: Luessen DJ 

PROVIDER: S-EPMC9372079 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature