Inhibition of potassium currents in outer hair cells and Deiters' cells from guinea pig cochlea by linopirdine.

To study the functional expression of KCNQ gene in outer hair cells (OHCs) and Deiters' cells, the effects of linopirdine on the whole cell K(+) current were investigated by using the whole cell variant of patch clamp technique in the present study. The outward tetraethylammonium (TEA)-sensitive K(+) current and the inward K(+) current (I(Kn)) in OHCs were recorded and measured before and after the administration of linopirdine. Simultaneously, the whole cell currents in Deiters?cells were also observed in normal solution and in the presence of linopirdine. After the application of 100 micromol/L linopirdine to OHCs, the peak K(+) current was reversibly blocked and the late K(+) current was partly reduced. In addition, the decay time constant of the TEA-sensitive K(+) current was prolonged in the presence of 100 micromol/L linopirdine. The inward current in OHCs was totally inhibited after the superfusion of 100 mmol/L and 200 micromol/L linopirdine respectively. The outward rectifier K(+) current (Ik) was the dominant K(+) current in the whole cell currents in Deiters' cells. In the presence of 200 micromol/L linopirdine, the I(K) current was not significantly affected. Our findings demonstrate that the KCNQ heteromeric or homomeric potassium channel is possibly the molecular basis for the peak outward K(+) current and that the inward I(Kn) current is mediated by KCNQ potassium channel. KCNQ potassium channel in OHCs can not only permit the K(+) efflux but also limit the depolarization. In the present study, no expression of KCNQ potassium channel is found in Deiters' cells.