NMDA receptor signaling in oligodendrocyte progenitors is not required for oligodendrogenesis and myelination
Open accessAbstract
Oligodendrocyte precursor cells (OPCs) express NMDA receptors (NMDARs) and form synapses with glutamatergic neurons throughout the CNS. Although glutamate influences the proliferation and maturation of these progenitors in vitro, the role of NMDAR signaling in oligodendrogenesis and myelination in vivo is not known. Here, we investigated the consequences of genetically deleting the obligatory NMDAR subunit NR1 from OPCs and their oligodendrocyte progeny in the CNS of developing and mature mice. NMDAR-deficient OPCs proliferated normally, achieved appropriate densities in gray and white matter, and differentiated to form major white matter tracts without delay. OPCs also retained their characteristic physiological and morphological properties in the absence of NMDAR signaling and were able to form synapses with glutamatergic axons. However, expression of calcium-permeable AMPA receptors (AMPARs) was enhanced in NMDAR-deficient OPCs. These results suggest that NMDAR signaling is not used to control OPC development but to regulate AMPAR-dependent signaling with surrounding axons, pointing to additional functions for these ubiquitous glial cells.
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NMDA receptors are not essential for myelination per se.
“This suggests that NMDA receptors are not essential for myelination per se”
From Oligodendroglial NMDA receptors regulate glucose import and axonal energy metabolism (2016) · cites this paper as De Biase et al., 2011
Deletion of NR1 in OPC did not reveal early functions of glutamate signaling.
“the early functions of glutamate signaling were not revealed by the deletion of NR1 in OPC”
From Oligodendroglial NMDA receptors regulate glucose import and axonal energy metabolism (2016) · cites this paper as De Biase et al., 2011
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- Authors
- De Biase, L. M., Kang, S. H., Baxi, E. G., Fukaya, M., Pucak, M. L., Mishina, M., Calabresi, P. A., & Bergles, D. E.
- Affiliations
- Johns Hopkins University (US)
- Kitasato University (JP)
- The University of Tokyo (JP)
- Corresponding author
- Bergles, Dwight E.
- ORCID
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2011-08-31
- Volume
- 31
- Issue
- 35
- Pages
- 12650-12662
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3179911
- OpenAlex
- W2002939398
- Cited by
- 161
- References
- 66
- Citations by year
- 2026: 7 · 2025: 7 · 2024: 9 · 2023: 3 · 2022: 6 · 2021: 12 · 2020: 10 · 2019: 12 · 2018: 9 · 2017: 14 · 2016: 18 · 2015: 16 · 2014: 9 · 2013: 18 · 2012: 8
- FWCI
- 3.88
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Maryland Stem Cell Research Fund
- National Institutes of Health
- Japan Society for the Promotion of Science (22123008, 21249012)
- National Institute of Mental Health (P50MH084020, MH-084020)
- National Eye Institute (T32EY017203)
- National Institute of Neurological Disorders and Stroke (NS051509, P30NS050274, R01NS051509)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- NMDA receptor signaling, oligodendrocyte precursor cells, oligodendrogenesis, myelination, NR1 subunit, calcium-permeable AMPA receptors, glutamatergic synapses, OPC proliferation, OPC differentiation, white matter tracts, glial development
- MeSH terms
- Autophagy-Related Proteins, Aldehyde Dehydrogenase 1 Family, Age Factors, Analysis of Variance, Animals, Animals, Newborn, Biophysics, Brain, Bromodeoxyuridine, Cell Differentiation, Electric Stimulation, Myelin Basic Protein, Glial Fibrillary Acidic Protein, Isoenzymes, Luminescent Proteins, Mice, Transgenic, Oligodendroglia, Stem Cells, Synapses, Signal Transduction, Receptors, N-Methyl-D-Aspartate, Receptors, Atrial Natriuretic Factor, Patch-Clamp Techniques, Gene Expression Regulation, Developmental, Glutamic Acid, Excitatory Postsynaptic Potentials, Receptor, Platelet-Derived Growth Factor alpha, Intracellular Signaling Peptides and Proteins, Cell Proliferation, Retinal Dehydrogenase, Mice, Basic Helix-Loop-Helix Proteins, In Vitro Techniques
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