A deficiency of the GluN2C subunit of the N-methyl-D-aspartate receptor is neuroprotective in a mouse model of ischemic stroke

Absence of the GluN2C subunit from the N-methyl-D-aspartate pool of ion channels diminished neuroedema in a murine model of ischemic stroke. The penumbral neurons of the core infarct of the GluN2C-/- mice showed diminished cytoskeletal disruption, decreased tauopathy, and increased phosphorylation of the pro-survival CREB molecule compared to WT mice. Thus, the GluN2C subunit impairs stroke-mediated neurological deficits, thereby, making the GluN2C subunit an attractive therapeutic target.177