Micro and macro-mechanics of the mammalian cochlea.

摘要

This thesis tackles issues in cochlear mechanics both at the microscopic and macroscopic level. Insights gained from the microscopic models are used to mathematically represent the microstructures in a macroscopic model of the cochlea. A comprehensive two-state Boltzmann model is developed for outer hair cell (OHC) motility and is validated by comparing its predictions with experimental findings. Issues with modeling outer hair cells (OHCs) are also discussed and their impact on in vivo behavior of OHCs is explored through simpler OHCs model that retain fidelity over the small voltage and strain variations seen in vivo. Models and parameters for other micro-structures are developed or adapted based on an extensive literature search on their properties. These models for the micro-structures are combined with a two-duct fluid model and cable models for electrical conduction to produce a global mathematical representation of the physiology of the cochlea. The equations are solved using the finite element method.; The parameters used in the model are almost entirely based on guinea pig data. The model predictions match a number of experimental results, both quantitatively and qualitatively. Model results for acoustic simulation and electrical stimuli are presented. Analysis of the model and its results gives fresh insight into the mechanics of the cochlea. Results indicate that the characteristic frequency at a location is determined predominantly by properties of the tectorial membrane, and not of the basilar membrane. This finding contradicts he conventional view in cochlear mechanics. The model is used to reinterpret certain experimental findings in past publications to provide experimental evidence for the new theory. The model results also show that the high frequency voltage roll-off of OHCs does not preclude force production from OHCs in the cochlea. The model necessitates transducer currents that are possibly higher than currents in vivo to achieve physiologically similar amplification. This leaves open the possibility that HB motility might be aiding force production. The model however rules out the possibility of HB force production being the sole active mechanism in the organ.