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 Ca2+ and shifted to 38+/-0.2 mV at 20 muM intracellular free Ca2+ (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(+)much greater thanCs(+)>Na+ (n=5-17). The whole-cell currents were inhibited by extracellular tetraethylammonium and iberiotoxin (IbTx) with IC50 values of 0.07 mM and 0.013 muM, 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 similar to6 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. (C) 2003 Published by Elsevier B.V.