Abstract
Recent studies on animal models have shown that noise exposure that does not lead to permanent threshold shift (PTS) can cause considerable damage around the synapses between inner hair cells (IHCs) and type-I afferent auditory nerve fibers (ANFs). Disruption of these synapses not only disables the innervated ANFs but also results in the slow degeneration of spiral ganglion neurons if the synapses are not reestablished. Such a loss of ANFs should result in signal coding deficits, which are exacerbated by the bias of the damage toward synapses connecting low-spontaneous-rate (SR) ANFs, which are known to be vital for signal coding in noisy background. As there is no PTS, these functional deficits cannot be detected using routine audiological evaluations and may be unknown to subjects who have them. Such functional deficits in hearing without changes in sensitivity are generally called “noise-induced hidden hearing loss (NIHHL).” Here, we provide a brief review to address several critical issues related to NIHHL: (1) the mechanism of noise induced synaptic damage, (2) reversibility of the synaptic damage, (3) the functional deficits as the nature of NIHHL in animal studies, (4) evidence of NIHHL in human subjects, and (5) peripheral and central contribution of NIHHL.
Highlights
Noise-induced hidden hearing loss (NIHHL) refers to any functional impairment seen in subjects with noise exposing history but no permanent threshold shift (PTS)
Noise exposures that result in only a temporary threshold shift (TTS) have a reversible impact on outer hair cells (OHCs) function, which is manifested by the recovery of otoacoustic emissions (OAE) [4,5,6] and cochlear microphonics (CM) [7,8,9,10,11]
When the damage occurs at both OHCs and the inner hair cells (IHCs)-spiral ganglion neurons (SGNs) synapses, the reduction of compound action potentials (CAP) amplitude is seen across all sound levels
Summary
Our studies on guinea pigs have revealed a clear recovery in the synapse count following a massive initial loss induced by noise exposure that did not lead to PTS [22, 23] This recovery was not complete, approximately 50% of the initial loss of paired ribbon and postsynaptic density (PSD) puncta in the basal half of the cochleae was seen 1 day after noise, and the loss was recovered to
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