Abstract Details
| Presented By: | Breneman, Kathryn |
| Affiliated with: | University of Utah, Bioengineering |
| Authors: | K.D. Breneman, R.D. Rabbitt |
| From: | University of Utah, Marine Biological Lab |
Title
Abstract
Hair cells of the inner ear are responsible for our sensation of hearing and balance. These cells have a bundle of microvilli-like nanotubes, called stereocilia, located at their apex. During stimulation, sound or postural changes generate a cascade that results in the stereocilia bundles being pivoted left and right. As they are pivoted, mechanically gated ion channels are opened and closed generating depolarization (excitation) and hyperpolarization (inhibition), respectively. An amplification mechanism, ubiquitous to all hair cells across all species, has been identified in the stereocilia bundle but the source it’s power remains a subject of debate. Recent results implicate flexoelectricity of the stereocilium membrane as an electrical to mechanical power conversion mechanism. Flexoelectricity, similar to piezoelectricity, relates changes in transmembrane potential across the lipid bilayer changes in the radius of curvature of the membrane. This leads to small length changes that, because the stereocilia are transversely coupled and graded in height, produce transverse deflections of the bundle. The present work addresses the role of hair bundle morphology in coupling flexoelectric changes in length to transverse hair bundle movements. There are a variety of bundle morphologies existent in nature ranging from the characteristic “W” shaped, 3 row morphology seen on mammalian cochlear outer hair cells, to circular or hexagonal arrays present on vestibular and non-mammalian auditory hair cells. A finite element model was composed to estimate flexoelectric axial length changes for a single stereocilium, and coupled to a two-dimensional kinematic model of the bundle to investigate how various morphologies appearing in nature might utilize this flexoelectric movement for amplification. [Supported by NIH R01-DC0006685].