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AMPA receptors shape Ca 2+ responses in cortical oligodendrocyte progenitors and CG‐4 cells
Author(s) -
Holtzclaw L. A.,
Gallo V.,
Russell J. T.
Publication year - 1995
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490420114
Subject(s) - ampa receptor , kainate receptor , glutamate receptor , oligodendrocyte , metabotropic glutamate receptor , microbiology and biotechnology , neuroscience , long term depression , biology , chemistry , receptor , biochemistry , central nervous system , myelin
Abstract Intracellular calcium signals triggered by glutamate receptor activation were studied in primary cortical oligodendrocyte lineage cells and in the oligodendrocyte cell line CG‐4. Glutamate, kainate, and AMPA (30‐300 μM) increased [Ca 2+ ] i in both types of cells at the stage of oligodendrocyte progenitors (O‐2A; GD3 + ) or pro‐oligodendroblasts (04 + ). The peak amplitude of Ca 2+ responses to glutamate receptor agonists was significantly larger in cortical cells. In CG‐4 and in cortical cells, the majority (more than 90%) of bipolar GD3 + or multipolar 04 + cells responded to kamate. In all the cells analyzed, kainate was more efficacious than AMPA and glutamate. The percentage of bipolar or multipolar cells responding to glutamate was significantly lower in the CG‐4 cell line than in primary cultures. Cellular responses typical of metabotropic glutamate receptor activation were observed in 20% of the cortical O‐2A progenitors, but in none of the CG‐4 cells. The AMPA‐selective antagonist GYKI 52466 blocked kainate‐induced Ca 2+ responses in cortical O‐2A cells. The selective AMPA receptor modulator cyclothiazide (30 μM) greatly potentiated the effects of AMPA (30‐100 μM) on [Ca 2+ ] i in cortical and CG‐4 cells. Our findings indicate that Ca 2+ responses in cells of the oligodendrocyte lineage are primarily shaped by functional AMPA receptors. © 1995 Wiley‐Liss, Inc. This article is a US Government work and, as such, is in the public domain in the United States of America.