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.
The Journal of Membrane Biology – Springer Journals
Published: Jun 1, 2003
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