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Oligodendrocyte progenitor cell proliferation and lineage progression are regulated by glutamate receptor-mediated K+ channel block

V Gallo, JM Zhou, CJ McBain, P Wright, PL Knutson and RC Armstrong
Journal of Neuroscience 15 April 1996, 16 (8) 2659-2670; DOI: https://doi.org/10.1523/JNEUROSCI.16-08-02659.1996
V Gallo
Laboratory of Cellular and Molecular Neurophysiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 202892, USA.
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JM Zhou
Laboratory of Cellular and Molecular Neurophysiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 202892, USA.
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CJ McBain
Laboratory of Cellular and Molecular Neurophysiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 202892, USA.
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P Wright
Laboratory of Cellular and Molecular Neurophysiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 202892, USA.
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PL Knutson
Laboratory of Cellular and Molecular Neurophysiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 202892, USA.
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RC Armstrong
Laboratory of Cellular and Molecular Neurophysiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 202892, USA.
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Abstract

We have analyzed the role of glutamate and its receptors (GluRs) in regulating the development of oligodendrocytes. Activation of AMPA- preferring GluRs with selective agonists inhibited proliferation of purified cortical oligodendrocyte progenitor (O-2A) cells cultured with different mitogens, as measured by [3H]thymidine incorporation or bromodeoxyuridine staining. In contrast, activation of GABA or muscarinic receptors did not affect O-2A proliferation. Cell viability and apoptosis assays demonstrated that the inhibition of O-2A proliferation was not attributable to a cytotoxic action of GluR agonists, and was reversible. Activation of GluRs prevented lineage progression from the O-2A (GD3+/nestin+) stage to the prooligodendroblast (O4+) stage, but did not affect O-2A migration. Additional experiments examined the membrane ionic channels mediating these GluR activation effects. We found that proliferating O-2A cells expressed functional delayed rectifier K+ channels, which were absent in pro-oligodendroblasts. GluR agonists and the K+ channel blocker tetraethylammonium (TEA) strongly inhibited delayed rectifier K+ currents in O-2A cells. TEA reproduced the effects of GluR activation on O-2A proliferation and lineage progression in the same concentration range that blocked delayed rectifier K+ currents. These results indicate that glutamate regulates oligodendrogenesis specifically at the O-2A stage by modulating K+ channel activity.

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The Journal of Neuroscience: 16 (8)
Journal of Neuroscience
Vol. 16, Issue 8
15 Apr 1996
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Oligodendrocyte progenitor cell proliferation and lineage progression are regulated by glutamate receptor-mediated K+ channel block
V Gallo, JM Zhou, CJ McBain, P Wright, PL Knutson, RC Armstrong
Journal of Neuroscience 15 April 1996, 16 (8) 2659-2670; DOI: 10.1523/JNEUROSCI.16-08-02659.1996

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Oligodendrocyte progenitor cell proliferation and lineage progression are regulated by glutamate receptor-mediated K+ channel block
V Gallo, JM Zhou, CJ McBain, P Wright, PL Knutson, RC Armstrong
Journal of Neuroscience 15 April 1996, 16 (8) 2659-2670; DOI: 10.1523/JNEUROSCI.16-08-02659.1996
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