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Blockade of K + channels induced by AMPA/kainate receptor activation in mouse oligodendrocyte precursor cells is mediated by NA + entry
Author(s) -
Borges K.,
Kettenmann H.
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.490420416
Subject(s) - kainate receptor , ampa receptor , biophysics , pertussis toxin , chemistry , patch clamp , intracellular , blockade , receptor , microbiology and biotechnology , medicine , biology , endocrinology , biochemistry , glutamate receptor , g protein
AMPA/kainate receptor activation in cultured oligodendrocyte precursor cells from embryonic mouse cortex leads to a blockade of delayed rectifying K + currents. In the present study, we provide evidence using the patch‐clamp technique in the whole‐cell configuration that the mechanism linking kainate receptor activation and K + conductance blockade is due to the receptor‐mediated Na + entry: (1) The blockade was not observed in Na + ‐free bathing solution nor when intracellular [Na + ] was elevated by dialzying the cell with a pipette solution containing high [Na + ]. (2) Elevation of intracellular [Na + ] alone led to a blockade of outward currents in contrast to cells dialyzed by sucrose. High [Li + ] i also reduced the outward currents, and in Li + ‐containing bathing solution the kainate‐induced blockade of K + channels was more pronounced. Probably, Li + accumulates intracellularly after permeation through the receptor pore due to slower extrusion mechanisms. Experiments with GTPγS or GDPβS and pertussis toxin indicated that GTP‐binding protein‐mediated mechanisms were not of importance for the kainate‐induced K + conductance blockade. Our data suggest that in glial precursor cells AMPA/kainate receptor activation leads to an intracellular [Na + ] increase which blocks delayed rectifying K + channels. © 1995 Wiley‐Liss, Inc.