Abstract

Hair bundle displacements and receptor potentials were recorded from outer hair cells (OHCs) in organotypic cultures of the mouse cochlea during force steps applied to the bundles with a silica probe of known stiffness. The receptor potentials of some OHCs adapt for excitatory displacements and the time constants of receptor potential adaptation and hair bundle force relaxation for excitatory displacements are very similar. Thus in these OHCs, the receptor potentials correspond to the applied force for excitatory displacements. For inhibitory displacements, the receptor potentials correspond to hair bundle displacement. Some OHC receptor potentials are nonadapting and follow displacement in both the excitatory and inhibitory directions. The hair bundles of nonadapting OHCs are less stiff than those of adapting OHCs and nonadapting OHCs are an order of magnitude less sensitive to hair bundle displacement than adapting OHCs. In response to a combination of excitatory, tonic, hair bundle displacement and current injection, the receptor potentials of nonadapting OHCs decline as the membrane potential is made more positive and reverse near 0 mV. When the receptor potentials of adapting OHCs measured during current injection are compensated for constant input resistance and driving voltage across the transducer conductance, the receptor potential amplitude at the offset of the step displacement is independent of the level and polarity of the injected current. Before adaptation, at the onset of the step displacement of the hair bundle, the amplitude of the receptor potential increases as the injected current becomes more positive. For adapting OHCs, the receptor potential amplitude is a linear function of excitatory bundle displacement for amplitudes less than 50 nm. With negative, but not positive, current injection the receptor potentials at the onset of the displacement tend to saturate and the slope of the function decreases. This voltage dependent control of OHC transducer operating range is proposed to have a role in regulating the sensitivity of the cochlea.

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