Effects of 900 MHz electromagnetic fields exposure on cochlear cells' functionality in rats: Evaluation of distortion product otoacoustic emissions

A new auditory phenomenon has been identified in the acoustic impulse response of the human ear. Using a signal averaging technique, a study has been made of the response of the closed external acoustic meatus to acoustic impulses near to the threshold of audibility. Particular attention has been paid to the waveform of the response at post excitation times in excess of 5 ms. No previous worker appears to have extended observations into this region. The response observed after about 5 ms is not a simple extension of the initial response attributable to the middle ear. The oscillatory response decay time constant was found to change from approximately 1 ms to over 12 ms at about this time. The slowly decaying response component was present in all normal ears tested, but was not present in ears with cochlear deafness. This component of the response appears to have its origin in some nonlinear mechanism probably located in the cochlea, responding mechanically to auditory stimulation, and dependent upon the normal functioning of the cochlea transduction process. A cochlear reflection hypothesis received some support from these results.

Otoacoustic emissions measured in the external ear canal describe responses that the cochlea generates in the form of acoustic energy. For the convenience of discussing their principal features, emitted responses can be classified into several categories according to the type of stimulation used to evoke them. On this basis, four distinct but interrelated classes can be distinguished including spontaneous, transiently evoked, stimulus-frequency, and distortion-product otoacoustic emissions. The present review details the findings that have been described for each emission type according to this classification schema. Additionally, the known features of emitted responses are discussed for both normally hearing and hearing-impaired humans and experimental animals, and with respect to their potential clinical applications. The findings reviewed here clearly indicate that future studies of otoacoustic emissions will significantly increase our understanding of the basic mechanisms of cochlear function while, at the same time, provide a new and important clinical tool.

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.