Noise induced synaptopathy (NIS) and hidden hearing loss (NIHHL) have been hot topic in hearing research since a massive synaptic loss was identified in CBA mice after a brief noise exposure that did not cause permanent threshold shift (PTS) in 2009. Based upon the amount of synaptic loss and the bias of it to synapses with a group of auditory nerve fibers (ANFs) with low spontaneous rate (LSR), coding-in-noise deficit (CIND) has been speculated as the major difficult of hearing in subjects with NIS and NIHHL. This speculation is based upon the idea that the coding of sound at high level against background noise relies mainly on the LSR ANFs. However, the translation from animal data to humans for NIS remains to be justified due to the difference in noise exposure between laboratory animals and human subjects in real life, the lack of morphological data and reliable functional methods to quantify or estimate the loss of the afferent synapses by noise. Moreover, there is no clear, robust data revealing the CIND even in animals with the synaptic loss but no PTS. In humans, both positive and negative reports are available. The difficulty in verifying CINDs has led a re-examination of the hypothesis that CIND is the major deficit associated with NIS and NIHHL, and the theoretical basis of this idea on the role of LSR ANFs. This review summarized the current status of research in NIS and NIHHL, with focus on the translational difficulty from animal data to human clinicals, the technical difficulties in quantifying NIS in humans, and the problems with the SR theory on signal coding. Temporal fluctuation profile model was discussed as a potential alternative for signal coding at high sound level against background noise, in association with the mechanisms of efferent control on the cochlea gain.

Noise induced synaptopathy (NIS) has been researched extensively since a large amount of synaptic loss without permanent threshold shift (PTS) was found in CBA mice after a brief noise exposure. However, efforts to translate these results to humans have met with little success—and might not be possible since noise exposure used in laboratory animals is generally different from what is experienced by human subjects in real life. An additional problem is a lack of morphological data and reliable functional methods to quantify loss of afferent synapses in humans. Based on evidence for disproportionate synaptic loss for auditory nerve fibers (ANFs) with low spontaneous rates (LSR), coding-in-noise deficits (CIND) have been speculated to be the major difficulty associated with NIS without PTS. However, no robust evidence for this is available in humans or animals. This has led to a re-examination of the role of LSR ANFs in signal coding in high-level noise. The fluctuation profile model has been proposed to support a role for high-SR ANFs in the coding of high-level noise in combination with efferent control of cochlear gain. This study aimed to induce NIS by a low-level, intermittent noise exposure mimicking what is experienced in human life and examined the impact of the NIS on temporal processing under masking. It also evaluated the role of temporal fluctuation in evoking efferent feedback and the effects of NIS on this feedback.