Global Grin2a loss causes divergent impairments to PV+ and SST+ interneurons and alters gamma oscillations in prefrontal cortex
GluN2A loss appears to disrupt inhibitory networks through distinct cell-type-specific mechanisms-presynaptic dysfunction in PV<sup>+</sup> cells and postsynaptic enhancement from SST<sup>+</sup> cells. PV<sup>+</sup> dysfunction aligns with gamma synchrony impairments linked to SCZ cognitive flexibility, while SST<sup>+</sup> alterations may contribute to impaired feedback inhibition and sensory deficits. These findings clarify GluN2A's role in interneuron subtype function and network stability in SCZ.
Authors
- Kevin S. Jones (ORCID: https://orcid.org/0000-0001-5281-1591)
- Hassan Hosseini (ORCID: https://orcid.org/0000-0002-2702-6994)
- Sky Evans-Martin
Institutions
- University of Michigan (US)
Publication Details
- Journal
- Neurobiology of Disease
- Published
- 2025-05-26
- DOI
- https://doi.org/10.1016/j.nbd.2025.106977
- Citations
- 3
- Primary Topic
- Neural dynamics and brain function
- Type
- article
- Field-Weighted Citation Impact
- 4.29
Funders
- Broad Institute
- Stanley Center for Psychiatric Research, Broad Institute