Current Transients Associated with BK Channels in Human Glioma Cells

Current Transients Associated with BK Channels in Human Glioma Cells We have previously demonstrated the expression of BK channels in human glioma cells. There was a curious feature to the whole-cell currents of glioma cells seen during whole-cell patch-clamp: large, outward current transients accompanied repolarization of the cell membrane following an activating voltage step. This transient current, I transient, activated and inactivated rapidly (≈1 ms). The I-V relationship of I transient had features that were inconsistent with simple ionic current through open ion channels: (i) I transient amplitude peaked with a −80 mV voltage change and was invariant over a 200 mV range, and (ii) I transient remained large and outward at −140 mV. We provide evidence for a direct relationship of I transient to glioma BK currents. They had an identical time course of activation, identical pharmacology, identical voltage-dependence, and small, random variations in the amplitude of the steady-state BK current and I transient seen over time were often perfectly in phase. Substituting intracellular K+ with Cs+, Li+, or Na + ions reversibly reduced I transient and BK currents. I transient was not observed in recordings of other BK currents (hbr5 expressed in HEK cells and BK currents in rat neurons), suggesting I transient is unique to BK currents in human glioma cells. We conclude that I transient is generated by a mechanism related to the deactivation, and level of prior activation, of glioma BK channels. To account for these findings we propose that K+ ions are “trapped” within glioma BK channels during deactivation and are forced to exit to the extracellular side in a manner independent of membrane potential. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Membrane Biology Springer Journals

Current Transients Associated with BK Channels in Human Glioma Cells

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Publisher
Springer-Verlag
Copyright
Copyright © 2003 by Springer-Verlag New York Inc.
Subject
Philosophy
ISSN
0022-2631
eISSN
1432-1424
D.O.I.
10.1007/s00232-003-2019-7
Publisher site
See Article on Publisher Site

Abstract

We have previously demonstrated the expression of BK channels in human glioma cells. There was a curious feature to the whole-cell currents of glioma cells seen during whole-cell patch-clamp: large, outward current transients accompanied repolarization of the cell membrane following an activating voltage step. This transient current, I transient, activated and inactivated rapidly (≈1 ms). The I-V relationship of I transient had features that were inconsistent with simple ionic current through open ion channels: (i) I transient amplitude peaked with a −80 mV voltage change and was invariant over a 200 mV range, and (ii) I transient remained large and outward at −140 mV. We provide evidence for a direct relationship of I transient to glioma BK currents. They had an identical time course of activation, identical pharmacology, identical voltage-dependence, and small, random variations in the amplitude of the steady-state BK current and I transient seen over time were often perfectly in phase. Substituting intracellular K+ with Cs+, Li+, or Na + ions reversibly reduced I transient and BK currents. I transient was not observed in recordings of other BK currents (hbr5 expressed in HEK cells and BK currents in rat neurons), suggesting I transient is unique to BK currents in human glioma cells. We conclude that I transient is generated by a mechanism related to the deactivation, and level of prior activation, of glioma BK channels. To account for these findings we propose that K+ ions are “trapped” within glioma BK channels during deactivation and are forced to exit to the extracellular side in a manner independent of membrane potential.

Journal

The Journal of Membrane BiologySpringer Journals

Published: Jun 1, 2003

References

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