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A discussion moderated by the authors on the topic “Outer Hair Cells and Prestin” was held on 18 July 2011 at the 11th International Mechanics of Hearing Workshop in Williamstown, Massachusetts. The paper provides an edited transcript of the session.

The voltage‐dependent chloride‐channel blocker anthracene‐9‐carboxylic acid (9AC) has been found to reduce the imaginary but not the real part of the mechanical impedance of the organ of Corti, suggesting that the effective stiffness of outer hair cells (OHCs) is reduced by 9AC. To examine whether 9AC interacts directly with the motor protein prestin to reduce the membrane component of the impedance, the patch‐clamp technique in whole‐cell configuration was used to measure the nonlinear capacitance (NLC) of isolated OHCs and, as control, prestin‐transfected human embryonic kidney 293 (HEK293) cells. Extracellular application of 9AC significantly reduced the NLC of both OHCs and HEK293 cells. Intracellular 9AC did not influence the blocking effect of the extracellular applied drug. These results suggest that 9AC interacts directly with prestin, reducing the effective stiffness of the motor, and that the interaction is extracellular.

Estimation of the function of the cochlea in human is possible only by deduction from indirect measurements, which may be subjective or objective. Therefore, for basic research as well as diagnostic purposes, it is important to develop methods to deduce and analyse error sources of cochlear‐state estimation techniques. Here, we present a model of technical and physiologic error sources contributing to the estimation accuracy of hearing threshold and the state of the cochlear amplifier and deduce from measurements of human that the estimated standard deviation can be considerably below 6 dB. Experimental evidence is drawn from two partly independent objective estimation techniques for the auditory signal chain based on measurements of otoacoustic emissions.

Knowledge of the mechanical properties of the outer hair cell (OHC) is essential for understanding its electromechanical action. To provide insight into underlying mechanics, we developed a finite‐element‐model of the OHC. The model contains both an intracellular viscous fluid and a homogeneous shell‐like structure for the basolateral wall, including anisotropic viscoelastic material properties. We found that the viscosity of the intracellular fluid could not yield the frequency dependent behaviour of the measured impedance. Shear viscosity needed to be included in the basolateral wall to obtain an adequate representation. The required value of the dynamic viscosity is on the order of 103 mPa⋅s and, therefore, 1000 fold higher than for water. Furthermore, changing the compressibility of the basolateral wall from 106 to 109 Pa suggests that the impedance is not significantly affected by this parameter. Finally, our calculations indicate that up to at least 10 kHz the measured impedances result from passive mechanical properties of the OHC.

Our study is a contribution to the long lasting debate of how the cochlea transmits distortions of its nonlinear amplification processes from their generation sites to the stapes. We provide evidence for a slow‐wave interpretation of the Ren et al. experiments by means of numerical simulations of a nonlinear hydrodynamic model, which is basically a slow‐wave cochlea model. We show that the simulations qualitatively reproduce their experiments. The analysis suggests that the measurement sites of negative phase slope of the basilar‐membrane (BM) vibrations at the cubic distortion product frequency were inside the generation sites or apical to the generation sites.