Cited by 286Neurogenesis and neuroplasticity mechanismsNeuroscience and Neuropharmacology ResearchNeuroinflammation and Neurodegeneration Mechanisms

Excitability and synaptic communication within the oligodendrocyte lineage

Open access
De Biase, Lindsay M., Nishiyama, Akiko, Bergles, Dwight E.·2010·The Journal of Neuroscience

Abstract

The mammalian CNS contains an abundant, widely distributed population of glial cells that serve as oligodendrocyte progenitors. It has been reported that these NG2-immunoreactive cells (NG2(+) cells) form synapses and generate action potentials, suggesting that neural-evoked excitation of these progenitors may regulate oligodendrogenesis. However, recent studies also suggest that NG2(+) cells are comprised of functionally distinct groups that differ in their ability to respond to neuronal activity, undergo differentiation, and experience injury following ischemia. To better define the physiological properties of NG2(+) cells, we used transgenic mice that allowed an unbiased sampling of this population and unambiguous identification of cells in discrete states of differentiation. Using acute brain slices prepared from developing and mature mice, we found that NG2(+) cells in diverse brain regions share a core set of physiological properties, including expression of voltage-gated Na(+) (NaV) channels and ionotropic glutamate receptors, and formation of synapses with glutamatergic neurons. Although small amplitude Na(+) spikes could be elicited in some NG2(+) cells during the first postnatal week, they were not capable of generating action potentials. Transition of these progenitors to the premyelinating stage was accompanied by the rapid removal of synaptic input, as well as downregulation of AMPA and NMDA receptors and NaV channels. Thus, prior reports of physiological heterogeneity among NG2(+) cells may reflect analysis of cells in later stages of maturation. These results suggest that NG2(+) cells are uniquely positioned within the oligodendrocyte lineage to monitor the firing patterns of surrounding neurons.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1523/jneurosci.6000-09.2010

Cites

65 of 65 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
De Biase, L. M., Nishiyama, A., & Bergles, D. E.
Affiliations
  • University of Connecticut (US)
  • Johns Hopkins University (US)
Corresponding author
Bergles, Dwight E.
Venue
The Journal of Neuroscience
Published
2010-03-10
Volume
30
Issue
10
Pages
3600-3611
ISSN
  • 0270-6474 (ISSN-L)
  • 1529-2401
OpenAlex
W1999272226
Cited by
286
References
65
Citations by year
2026: 16 · 2025: 16 · 2024: 14 · 2023: 21 · 2022: 11 · 2021: 19 · 2020: 16 · 2019: 20 · 2018: 10 · 2017: 23 · 2016: 15 · 2015: 20 · 2014: 14 · 2013: 20 · 2012: 14
FWCI
7.18
Type
journal article
Language
en
Open access
Locations
  • Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Multiple Sclerosis Society
  • National Alliance for Research on Schizophrenia and Depression
  • Multiple Sclerosis Society
  • National Institutes of Health
  • U.S. Public Health Service (PAR-02-059)
  • National Eye Institute (T32EY017203)
  • National Institute of Neurological Disorders and Stroke (R01NS049267, NS-049267, 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
oligodendrocyte precursor cells, oligodendrocyte progenitors, oligodendrocyte lineage, action potential, voltage-gated sodium channels, ionotropic glutamate receptors, AMPA receptors, NMDA receptor, oligodendrogenesis, synaptic input, neuronal activity regulation, transgenic mice, brain development
MeSH terms
Chondroitin Sulfate Proteoglycan 4, Action Potentials, Animals, Animals, Newborn, Cell Communication, Membrane Proteins, Mice, Transgenic, Oligodendroglia, Chondroitin Sulfate Proteoglycans, Synapses, Cell Lineage, Gene Expression Profiling, Mice

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review