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Journal of Neuroscience, Vol 16, 519-530, Copyright © 1996 by Society for Neuroscience
Developmental regulation of the toxin sensitivity of Ca(2+)-permeable AMPA receptors in cortical glia
O Meucci, A Fatatis, JA Holzwarth and RJ Miller
Department of Pharmacological and Physiological Sciences, University of Chicago, Illinois 60637, USA.
We examined the properties of glutamate agonist-induced Ca2+ fluxes in
cultured CG-4 and O-2A progenitor cells from rat cortex. Kainate- induced
Ca2+ fluxes in these cells were found to be attributable to the activation
of AMPA receptors. Thus, these fluxes were enhanced by cyclothiazide but
not by concanavalin A and were blocked completely by GYKI-53655. We
simultaneously examined kainate-induced Ca2+ entry and Na+ currents in
these cells under voltage-clamp conditions. Both of these parameters were
blocked by Joro spider toxin (JSTx) in undifferentiated cells. However,
neither JSTx nor Argiotoxin 636 effectively blocked either parameter in
cells differentiated into type II astrocytes. This change in toxin
sensitivity occurred slowly over a period of several days. Similar results
were obtained in Ca(2+)-imaging studies. When cells were differentiated
into oligodendrocytes, they showed an intermediate sensitivity to block by
JSTx as assessed using imaging and voltage-clamp studies. Analysis of the
expression of AMPA- receptor subunits showed an increase in the
concentration of glutamate receptor-2 (GluR2) in CG-4 cells as they
differentiated into type II astrocytes and oligodendrocytes. These results
demonstrate that the AMPA receptors in cells of the O-2A lineage flux
appreciable amounts of Ca2+ but may contain variable amounts of edited
GluR2 subunits.
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