Cited by 551Neurogenesis and neuroplasticity mechanismsGlioma Diagnosis and TreatmentCongenital heart defects research

The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.

Progeny of Olig2-Expressing Progenitors in the Gray and White Matter of the Adult Mouse Cerebral Cortex

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Abstract

Despite their abundance, still little is known about the rather frequent, constantly proliferating progenitors spread throughout the adult mouse brain parenchyma. The majority of these progenitors express the basic-helix-loop-helix transcription factor Olig2, and their number further increases after injury. Here, we examine the progeny of this progenitor population by genetic fate mapping using tamoxifen-inducible Cre-recombination in the Olig2 locus to turn on permanent reporter gene expression in the adult brain. Consistent with Olig2 expression in proliferating NG2(+) progenitors, most reporter(+) cells seen shortly after initiating recombination at adult stages incorporated BrdU and contained the proteoglycan NG2 in both the gray (GM) and the white matter (WM) of the cerebral cortex. However, at longer time points after induction, we observed profound differences in the identity of reporter(+) cells in the WM and GM. Whereas most of the Olig2(+) progenitors had generated mature, myelinating oligodendrocytes in the WM, hardly any reporter(+) cells showing mature oligodendrocyte characteristics were detectable even up to 6 months after recombination in the GM. In the GM, most reporter(+) cells remained NG2(+), even after injury, but stopped proliferating rather soon after recombination. Thus, our results demonstrate the continuous generation of mature, myelinating oligodendrocytes in the WM, whereas cells in the GM generated mostly postmitotic NG2(+) glia.

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Crossref · 10.1523/jneurosci.2831-08.2008

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Metadata

Authors
Dimou, L., Simon, C., Kirchhoff, F., Takebayashi, H., & Götz, M.
Affiliations
  • Physiologisches Institut (DE)
  • Helmholtz Munich (DE)
  • Max Planck Society (DE)
  • National Institute for Physiological Sciences (JP)
  • Center for Integrated Protein Science Munich (DE)
Venue
The Journal of Neuroscience
Published
2008-10-08
Volume
28
Issue
41
Pages
10434-10442
ISSN
  • 0270-6474 (ISSN-L)
  • 1529-2401
OpenAlex
W2095490681
Cited by
551
References
51
Citations by year
2026: 19 · 2025: 19 · 2024: 22 · 2023: 30 · 2022: 26 · 2021: 38 · 2020: 45 · 2019: 35 · 2018: 32 · 2017: 35 · 2016: 33 · 2015: 40 · 2014: 42 · 2013: 36 · 2012: 23
FWCI
7.73
Type
journal article
Language
en
Open access
Locations
  • Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Max Planck Institute for Plasma Physics (submittedVersion)
  • Site cant be reached (submittedVersion)
  • MPG.PuRe (Max Planck Society) (submittedVersion)
Funders
  • European Commission
  • Deutsche Forschungsgemeinschaft
Topics
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Health Sciences › Medicine › Oncology › Glioma Diagnosis and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
Keywords
Olig2, cerebral cortex, gray matter, white matter, NG2 glia, oligodendrocyte differentiation, myelination, fate mapping, Cre recombination, BrdU labeling, brain injury, progenitor cell proliferation
MeSH terms
Oligodendrocyte Transcription Factor 2, Chondroitin Sulfate Proteoglycan 4, Animals, Antigens, Cell Differentiation, Cerebral Cortex, Mice, Inbred C57BL, Mitosis, Myelin Sheath, Nerve Tissue Proteins, Neuroglia, Oligodendroglia, Periaqueductal Gray, Proteoglycans, Stem Cells, Tamoxifen, Wounds, Stab, Gene Expression, Genes, Reporter, Integrases, Animals, Genetically Modified, Cell Proliferation, Mice, Basic Helix-Loop-Helix Proteins

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