Journal
CELL REPORTS
Volume 35, Issue 7, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2021.109147
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Funding
- National Multiple Sclerosis Society postdoctoral fellowship [FG 1927-A-1]
- Shriners Hospitals for Children postdoctoral fellowship [84298-PHI]
- NIH [R01GM117907, R21NS092009, R01NS089586]
- Deutsche Forschungsgemeinschaft [FOR2289-P8]
- Chica and Heinz Schaller Foundation
- Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
- National Multiple Sclerosis Society [PP1988]
- Ellison Medical Foundation [AG-NS-1101-13]
- Shriners Hospitals for Children [85500-PHI-14]
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Regulation of AMPAR GluA2 content in oligodendrocyte precursor cells affects cell proliferation and regenerative behavior, serving as a potential target for myelin repair.
Oligodendrocyte precursor cells (OPCs) are essential for developmental myelination and oligodendrocyte regeneration after CNS injury. These progenitors express calcium-permeable AMPA receptors (AMPARs) and form direct synapses with neurons throughout the CNS, but the roles of this signaling are unclear. To enable selective alteration of the properties of AMPARs in oligodendroglia, we generate mice that allow cell-specific overexpression of EGFP-GluA2 in vivo. In healthy conditions, OPC-specific GluA2 overexpression significantly increase their proliferation in an age-dependent manner but did not alter their rate of differentiation into oligodendrocytes. In contrast, after demyelinating brain injury in neonates or adults, higher GluA2 levels promote both OPC proliferation and oligodendrocyte regeneration, but do not prevent injury-induced initial cell loss. These findings indicate that AMPAR GluA2 content regulates the proliferative and regenerative behavior of adult OPCs, serving as a putative target for better myelin repair.
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