Animal Models of Noise-Induced Hearing Loss

Abstract

Animal models have played a major role in understanding noise-induced hearing loss, a major cause of hearing loss in industrialized societies. Behavioral models using positive and negative reinforcement techniques have played an important role in delineating the relationship between the physical characteristic of the noise, namely intensity, spectral content, and duration, and the magnitude of the resulting hearing loss. An important contribution from these studies was the discovery that the hearing loss reaches an asymptotic value of threshold shift for exposures lasting 24 h or more. Animal models of noise-induced hearing loss have revealed a significant loss of frequency sensitivity, making it difficult to discriminate signals in noise, and a breakdown in temporal resolution that makes it difficult to perceive the temporal information contained in complex signals such as speech. Animal models have shown that prolonged exposure to high-level noise mainly damages the sensory hair cells in the inner ear. The stereocilia bundles on the sensory hair cells, which contain the mechanically gated ion channels responsible for converting sound into neural activity, are especially vulnerable to acoustic overstimulation. High-level noise can obliterate or damage the stereocilia. More severe sound exposures can result in degeneration of the hair cell body, beginning with the outer hair cells followed by the inner hair cells. The functional status of the outer hair cells can be evaluated in noise-exposed animals using distortion product otoacoustic emissions. When healthy ears are stimulated with two primary tones, f 1 and f2, the inner ear generates a distortion tone, the most prominent of which occurs at 2f1–f2. Acoustic overstimulation that primarily damages the outer hair cells and leads to mild to moderate hearing loss almost completely abolishes the distortion product otoacoustic emission. The type I spiral ganglion neurons, which make synaptic contact with single inner hair cells, can be used to assess the functional status of a very narrow region of the cochlea. The functional status of small populations of type I neurons can be evaluated using tone bursts to elicit the compound action potential. Narrow band noise exposures that damage specific regions of the cochlea cause an increase in the compound action potential threshold at frequencies associated with the region of cochlear pathology. Microelectrode recordings from single type I auditory nerve fibers can be used to delineate the pathophysiology at specific sites along the cochlea. Sound exposures that selectively damage the outer hair cells lead to an elevation of threshold and loss of tuning. In cases in which acoustic overstimulation destroys both the outer hair cells and inner hair cells, nerve fibers associated with the damaged region are unresponsive to sound resulting in a dead region. The biological mechanisms that lead to noise-induced degeneration of hair cells is not fully understood, but there is growing awareness that hair cell death may be initiated by oxidative stress that leads to hair cell death by necrosis or apoptosis.Key WordsChinchillaGerbilMiceNoise exposureHearing lossTuningOxidative stressHair cellsAuditory nerve