Myelination by oligodendrocytes (OLs) is critical for rapid nerve signal conduction. Abnormalities of OLs mediate a variety of central nervous system (CNS) diseases, including multiple sclerosis. N-methyl-D-aspartate (NMDA) receptors are ionotropic glutamate receptors expressed in neurons and are key regulators for neuron survival and normal brain functions. Recently, NMDA receptors were identified in OLs and contribute to OL migration, differentiation and myelination. However, the exact function of NMDA receptors on OLs remains unclear. Previous studies have shown that GluN2C is one of the predominant NMDA receptor subunits expressed in OLs. Here we report that NMDA treatment promotes OL differentiation in vitro, but fails to increase mature OL percentage in the absence of GluN2C. In addition, we observed an early developmental myelination delay and long-term recovery in the optic nerve of GluN2C-knockout (KO) mice in vivo, which was closely related to the impairment of OL differentiation. Overall, these results indicate a functional involvement of GluN2C-containing NMDA receptors in OL differentiation and myelination.
Department of Neuroscience & Regenerative Medicine
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