Cited by 808Neurogenesis and neuroplasticity mechanismsNeuroinflammation and Neurodegeneration MechanismsNeonatal and fetal brain pathology

Oligodendrocyte progenitors balance growth with self-repulsion to achieve homeostasis in the adult brain

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Hughes, Ethan G, Kang, Shin H, Fukaya, Masahiro, Bergles, Dwight E·2013·Nature Neuroscience

Abstract

The adult CNS contains an abundant population of oligodendrocyte precursor cells (NG2(+) cells) that generate oligodendrocytes and repair myelin, but how these ubiquitous progenitors maintain their density is unknown. We generated NG2-mEGFP mice and used in vivo two-photon imaging to study their dynamics in the adult brain. Time-lapse imaging revealed that NG2(+) cells in the cortex were highly dynamic; they surveyed their local environment with motile filopodia, extended growth cones and continuously migrated. They maintained unique territories though self-avoidance, and NG2(+) cell loss though death, differentiation or ablation triggered rapid migration and proliferation of adjacent cells to restore their density. NG2(+) cells recruited to sites of focal CNS injury were similarly replaced by a proliferative burst surrounding the injury site. Thus, homeostatic control of NG2(+) cell density through a balance of active growth and self-repulsion ensures that these progenitors are available to replace oligodendrocytes and participate in tissue repair.

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  • 6-OHDA causes dopamine containing nerve terminals to degenerate, which leads to oligodendrocyte precursor cell infiltration.

    “6-OHDA causes dopamine containing nerve terminals to degenerate, which leads to oligodendrocyte precursor cell infiltration.24,25”

    From Characterization of a novel adeno-associated viral vector with preferential oligodendrocyte tropism (2016) · cites this paper as [24]

    The Introduction (page unavailable) says NG2+ cell proliferation increases in chronic neurodegenerative disease, but does not address 6-OHDA, degeneration of dopamine-containing terminals, or precursor-cell infiltration after that degeneration. Searches for 6-OHDA and dopaminergic terminal degeneration found no passage establishing the claimed sequence. (LLM, conf=0.76)

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Authors
Hughes, E. G., Kang, S. H., Fukaya, M., & Bergles, D. E.
Affiliations
Johns Hopkins University (US)
Corresponding author
Bergles, Dwight E
Venue
Nature Neuroscience
Published
2013-04-28
Volume
16
Issue
6
Pages
668-676
ISSN
  • 1097-6256 (ISSN-L)
  • 1546-1726
OpenAlex
W2059276463
Cited by
808
References
56
Citations by year
2026: 41 · 2025: 53 · 2024: 65 · 2023: 66 · 2022: 62 · 2021: 92 · 2020: 70 · 2019: 71 · 2018: 61 · 2017: 70 · 2016: 48 · 2015: 47 · 2014: 51 · 2013: 10
FWCI
19.28
Type
journal article
Language
en
Open access
Locations
  • Nature Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of Neurological Disorders and Stroke (NS050274, F32NS076098, NS051509, P30NS050274, R01NS051509)
Topics
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
Keywords
oligodendrocyte precursor cells, cell proliferation, cell migration, cell death, cell differentiation, filopodia, growth cones, central nervous system injury, remyelination, adult brain, cortical progenitors
MeSH terms
Animals, Cell Count, Cell Differentiation, Cell Movement, Cerebral Cortex, Homeostasis, Mice, Transgenic, Oligodendroglia, Cell Death, Cell Proliferation, Mice, Neural Stem Cells, Time-Lapse Imaging

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