BK channels mediate the voltage-dependent outward current in type I spiral ligament fibrocytes.
Recent experimental and clinical studies have provided considerable evidence to support the phenomenon of K(+) recycling in the mammalian cochlea. However, the precise cellular and molecular mechanisms underlying and regulating this process remain only partially understood. Here, we report that cultured type I spiral ligament fibrocytes (SLFs), a major component of the K(+) recycling pathway, have a dominant K(+) membrane conductance that is mediated by BK channels. The averaged half-maximal voltage-dependent membrane potential for the whole-cell currents was 70+/-1.2 mV at 1 nM intracellular free Ca(2+) and shifted to 38+/-0.2 mV at 20 microM intracellular free Ca(2+) (n=4-6). The reversal potential of whole-cell tail currents against different bath K(+) concentrations was 52 mV per decade (n=3-6). The sequence of relative ion permeability of the whole-cell conductance was K(+)>Rb(+)z.Gt;Cs(+)>Na(+) (n=5-17). The whole-cell currents were inhibited by extracellular tetraethylammonium and iberiotoxin (IbTx) with IC(50) values of 0.07 mM and 0.013 microM, respectively (n=3-7). The membrane potentials of type I SLFs measured with conventional zero-current whole-cell configuration were highly K(+)-selective and sensitive to IbTx (n=4-9). In addition, the BK channels in these cells exhibited voltage-dependent and incomplete inactivation properties and the recovery time was estimated to be approximately 6 s with repetitive voltage pulses from -70 to 80 mV (n=3). These data suggest that BK channels in type I SLFs play a major role in regulating the intracellular electrochemical gradient in the lateral wall syncytium responsible for facilitating the K(+) movement from perilymph to the stria vascularis.
Shen
Zhijun
Z
Department of Pathology and Laboratory Medicine, Medical University of South Carolina, 165 Ashley Avenue, P.O. Box 250908, Charleston, SC 29425, USA. shenz@musc.edu
Liang
Fenghe
F
Hazen-Martin
Debra J
DJ
Schulte
Bradley A
BA
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002412:Cations / Q000378:metabolism; D002478:Cells, Cultured; D003051:Cochlea / Q000166:cytology / Q000502:physiology*; D004553:Electric Conductivity; D005260:Female; D005849:Gerbillinae; D007425:Intracellular Membranes / Q000378:metabolism; D051036:Large-Conductance Calcium-Activated Potassium Channels; D008022:Ligaments / Q000166:cytology / Q000502:physiology*; D008297:Male; D008564:Membrane Potentials; D009994:Osmolar Concentration; D010455:Peptides / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism; D026902:Potassium Channel Blockers / Q000494:pharmacology; D024681:Potassium Channels, Calcium-Activated / Q000037:antagonists & inhibitors / Q000502:physiology*; D019789:Tetraethylammonium / Q000494:pharmacology
D002412:Cations; D051036:Large-Conductance Calcium-Activated Potassium Channels; D010455:Peptides; D026902:Potassium Channel Blockers; D024681:Potassium Channels, Calcium-Activated; D019789:Tetraethylammonium; C064719:iberiotoxin; D011188:Potassium; D002118:Calcium