MEMBRANE TENSION DIRECTLY SHIFTS VOLTAGE-DEPENDENCE OF OUTER HAIR CELL MOTILITY AND ASSOCIATED GATING CHARGE

The unique electromotility of the outer hair cell (OHC) is believed to promote sharpening of the passive mechanical vibration of the mammali an basilar membrane. The cell also presents a voltage-dependent capaci tance, or equivalently, a nonlinear gating current, which correlates w ell with its mechanical activity, suggesting that membrane-bound volta ge sensor-motor elements control OHC length. We report that the voltag e dependence of the gating charge and motility are directly related to membrane stress induced by intracellular pressure. A tracking procedu re was devised to continuously monitor the voltage at peak capacitance (V-pkCm) after obtaining whole cell voltage clamp configuration. In a ddition, nonlinear capacitance was more fully evaluated with a stair s tep voltage protocol. Upon whole cell configuration, V-pkCm was typica lly near -20 mV. Negative patch pipette pressure caused a negative shi ft in V-pkCm, which obtained a limiting value near the normal resting potential of the OHC (similar to-70 mV) at the point of cell collapse. Positive pressure in the pipette caused a positive shift that could r each values greater than 0 mV. Measures of the mechanical activity of the OHC mirrored those of charge movement. Similar membrane-tension de pendent peak shifts were observed after the cortical cytoskeletal netw ork was disrupted by intracellular dialysis of trypsin from the patch pipette. We conclude that unlike stretch receptors, which may sense te nsion through elastic cytoskeletal elements, the OHC motor senses tens ion directly. Furthermore, since the voltage dependence of the OHC non linear capacitance and motility is directly regulated by intracellular turgor pressure, we speculate that modification of intracellular pres sure in vivo provides a mechanism for controlling the gain of the mamm alian ''cochlear amplifier''.