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A Ca 2+ ‐ and pH‐Dependent K + Channel of rat C6 glioma cells and its possible role in acidosis‐induced cell swelling
Author(s) -
Strupp Michael,
Staub Frank,
Grafe Peter
Publication year - 1993
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.440090207
Subject(s) - quinidine , depolarization , biophysics , acidosis , conductance , electrophysiology , membrane potential , biology , swelling , endocrinology , pharmacology , neuroscience , medicine , pathology , mathematics , combinatorics
The aim of the present study was to explore whether a change in membrane K + conductance contributes to acidosis‐induced swelling of cultured rat C6 glioma cells. Electrophysiological studies were perfomed using whole‐cell and single‐channel recordings in combination with cell volume measurements in cell suspension by flow cytometry. Whole‐cell recordings revealed a voltage‐dependent K + conductance. The predominant K + channel in single‐channel recordings with symmetrical high K + concentrations was inwardly rectifying and had conductances of 35 and 15 pS, respectively. A raised internal free Ca 2+ concentration and membrane depolarization increased the open probability of this channel. Internal acidosis (pH 6.4−5.4), on the other hand, reduced open probability and single‐channel conductance. Both whole‐cell and single‐channel K + currents were blocked by quinidine (0.1−1 mM), which was therefor used to analyze the functional consequences of an inhibition of this conductance for volume. Thereby, quinidine (1 mM) produced a small (5%) and transient cell swelling of C6 glioma cells. In contrast, acidosis (pH 5.6) caused a much larger (about 20%) and maintained swelling. Since quinidine produced only a minor swelling of C6 cells, it is unlikely that inhibition of the K + conductance caused acidosis‐induced cell swelling. Other mechanisms, such as activation of ion transporters, must therefore be responsible. © 1993 Wiley‐Liss, Inc.