Current Transients Associated with BK Channels in Human Glioma Cells |
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Authors: | C B?Ransom X?Liu Email author" target="_blank">H?SontheimerEmail author |
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Institution: | (1) Department of Neurobiology, University of Alabama at Birmingham, Birmingham, AL, USA |
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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. |
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Keywords: | Large-conductance calcium-activated K+ channel Glia Permeation Patch clamp |
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