SUMMARY
The mammalian ear is a complex biological system that can detect sound signals and amplify theresponse to low-level sounds. The active amplification, also known as the “ cochlear amplifier” is driven by electromotility of outer hair cells (OHCs). This research focus on two distinct aspects of cochlear mechanics. The first contribution of this research is the implementation, calibration and improvement of computational efficiency of the cochlear model for predictions on the sound evoked response of the cochlea and of the generation of otoacoustic emissions. A physiologically-motivated gerbil cochlear model with electrical longitudinal coupling is calibrated to capture the nonlinear measurement in extracellular OHC voltage. The model is then used to examine distortion product otoacoustic emissions (DPOAEs), a sound signal that can be detected in the ear canal in response to two-tone stimulus. DPOAE measurement often serves as a noninvasive approach to probe cochlear function in clinical applications. This research also examines the generation and propagation mechanism of intracochlear distortion products (IDPs). The influence of primary frequency ratio on IDP generation and propagation is examined by comparing model simulations to experimental measurement. The results show that IDPs are broadly generated but their contribution to DPOAEs are spatially restricted. A nonlinear frequency domain model is implemented to significantly improve the speed of simulation. The second aspect of the research focuses on the influence of genetic mutations on material properties of mouse tectorial membrane (TM), which is an extracellular matrix located above OHCs. This research aims to examining the effect of genetic mutation on anisotropic material properties of TM in wild-type and transgenic mice. A computational TM model with viscous boundary layer was employed to determine the material properties of the mouse TM by using an inverse fitting methodology to wave propagation measured on isolated TM segments. Results indicate that genetic mutation affects stiffness and damping properties of the tectorial membrane, which may influence the OHC electromechanical functionality and normal hearing ability.