Abstract
Noise-induced synaptopathy and relevant hidden hearing loss (NIS and NIHHL) have been a hot topic in hearing research for almost 15 years. The progress is summarized in this review to address the reversibility of the synaptic damage after the initial loss, and the role of functional deficit in the repaired synapses as the reason for hearing impairment in addition to the deafferentiation caused by the synaptic loss, per se. The evidence supporting the synaptic repair is summarized. It is pointed out that coding-in-noise deficit (CIND) may not be the major problem of NIS and NIHHL, since solid evidence supporting the existence of this deficit is not available even in animal studies, as well as in in human reports. Rather, temporal processing deficits are clearly demonstrated in subjects with NIS and potentially NIHHL. The idea of CIND as the major concern in NIHHL is proposed based upon the functional categorization of the auditory nerve (ANF) by spontaneous rate and the biased loss of the ribbon synapses innervation the low-SR ANF. The limitation of this hypothesis is discussed in detail. The review also addresses the difficulty of translating animal data to humans and the need for new research in the future.