Outer Hair Cell Electromotility and Otoacoustic Emissions

Abstract

Outer hair cell electromotility is a rapid, force generating, length change in response to electrical stimulation. DC electrical pulses either elongate or shorten the cell and sinusoidal electrical stimulation results in mechanical oscillations at acoustic frequencies. The mechanism underlying outer hair cell electromotility is thought to be the origin of spontaneous otoacoustic emissions. The ability of the cell to change its length requires that it be mechanically flexible. At the same time the structural integrity of the organ of Corti requires that the cell possess considerable compressive rigidity along its major axis. Evolution appears to have arrived at novel solutions to the mechanical requirements imposed on the outer hair cell. Segregation of cytoskeletal elements in specific intracellular domains facilitates the rapid movements. Compressive strength is provided by a unique hydraulic skeleton in which a positive hydrostatic pressure in the cytoplasm stabilizes a flexible elastic cortex with circumferential tensile strength. Cell turgor is required in order that the pressure gradients associated with the electromotile response can be communicated to the ends of the cell. A loss in turgor leads to loss of outer hair cell electromotility. Concentrations of salicylate equivalent to those that abolish spontaneous otoacoustic emissions in patients weaken the outer hair cell's hydraulic skeleton. There is a significant diminution in the electromotile response associated with the loss in cell turgor. Aspirin's effect on outer hair cell electromotility attests to the role of the outer hair cell in generating otoacoustic emissions and demonstrates how their physiology can influence the propagation of otoacoustic emissions. THERE HAS BEEN a dramatic change in our understanding of the biophysics of the mammalian inner ear over the past decade. The concept of the cochlea as a passive organ that converts the mechanical vibrations of sound into neural energy has been altered by the startling finding that outer hair cells possess a unique electromotile capacity (Brownell, 1983 ;1984 ;Brownell, Bader, Bertrand, & de Ribaupierre, 1985). The electromotility appears to be responsible for the cochlea's surprising ability to generate sound (Kemp, 1978; see also other articles in this issue). The hearing science community now accepts the presence of otoacoustic emissions after nearly a decade of experimental confirmation. Skepticism from the more general sensory science community is understandable. The fact that the ear can make sound is, at one level, equivalent to the eye producing light or the nose expelling odors. Energy conversion in both directions (bidirectional transduction) appears unique to hearing and is thought to contribute to the remarkable sensitivity and exquisite frequency selectivity of mammalian hearing. This contribution is discussed below in a brief review of the evidence implicating outer hair cells in generating otoacoustic emissions. The physiological characteristics of outer hair cell electro...

Inner ear drug delivery via a reciprocating perfusion system in the guinea pig

“…Salicylates are well known to interfere with outer hair cell electromotility [31] and would be expected, therefore, to alter both DPOAEs and CAPs (with CAP alteration secondary to an effect on the hair cell). Consistent with this expectation, salicylate altered both CAP thresholds and low-level iso-DPOAEs, as displayed in Fig.…”

Estudo das emissões otoacústicas por produto de distorção durante a hipotermia em humanos

“…OAEs, described by Kemp in 1978 14 , arise apparently in the OHC 2,15,16 and possibly represent the rapid contractions of this cell group. They are acoustic phenomena of cochlear nature, which reverberate through the ossicles in the middle ear and are transmitted to the ear canal, where they can be captured through a microphone.…”

Role of Transient Evoked Otoacoustic Emission Beyond Screening of Hearing Impairment: A Study of 400 Cases

“…The prevalence of hearing disorders as per various studies is [1] WHO 1967, 0.1 %; [2] BIRREL.J.F. 1986, 0.12 %; [3] FRASER.G.R.…”

“…The electro motility of the OHCs has a feedback effect on the basilar membrane, causing it to vibrate. Therefore, the electromotility of the OHCs is thought to be the mechanism which underlies OAEs [2,7]. Using OAEs to monitor ototoxic medications is logical.…”