Document Detail


Excitability and synaptic communication within the oligodendrocyte lineage.
MedLine Citation:
PMID:  20219994     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Lindsay M De Biase; Akiko Nishiyama; Dwight E Bergles
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  30     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-03-11     Completed Date:  2010-04-09     Revised Date:  2014-09-20    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3600-11     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Action Potentials / genetics,  physiology
Animals
Animals, Newborn
Cell Communication* / genetics,  physiology
Cell Lineage* / genetics,  physiology
Chondroitin Sulfate Proteoglycans / biosynthesis*,  genetics*
Gene Expression Profiling
Membrane Proteins / biosynthesis*,  genetics*
Mice
Mice, Transgenic
Oligodendroglia / cytology,  metabolism,  physiology*
Synapses* / genetics,  physiology
Grant Support
ID/Acronym/Agency:
NS049267/NS/NINDS NIH HHS; NS051509/NS/NINDS NIH HHS; P30 NS050274/NS/NINDS NIH HHS; P30 NS050274-039003/NS/NINDS NIH HHS; PAR-02-059//PHS HHS; R01 NS049267/NS/NINDS NIH HHS; R01 NS049267-03/NS/NINDS NIH HHS; R01 NS051509/NS/NINDS NIH HHS; R01 NS051509-03/NS/NINDS NIH HHS; T32 EY017203/EY/NEI NIH HHS
Chemical
Reg. No./Substance:
0/CSPG4 protein, human; 0/Chondroitin Sulfate Proteoglycans; 0/Membrane Proteins
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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