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Journal of Neuroscience, Vol 16, 2659-2670, Copyright © 1996 by Society for Neuroscience
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
Laboratory of Cellular and Molecular Neurophysiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 202892, USA.
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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