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Neural Plasticity
Volume 2016, Article ID 6143164, 9 pages
http://dx.doi.org/10.1155/2016/6143164
Review Article

Cochlear Synaptopathy and Noise-Induced Hidden Hearing Loss

1Department of Physiology, Medical College of Southeast University, 87 Dingjiaoqiao Road, Nanjing 210009, China
2School of Human Communication Disorders, Dalhousie University, 1256 Barrington St. Dalhousie University, Halifax, NS, Canada B3J 1Y6

Received 30 May 2016; Revised 9 August 2016; Accepted 21 August 2016

Academic Editor: Preston E. Garraghty

Copyright © 2016 Lijuan Shi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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.