The concept of ?hidden? hearing loss challenges the idea that temporary threshold shifts (TTS) reflect a return to normal hearing. Recent studies indicate that after noise-exposure that produces TTS, and thus clinically 'normal' audiograms, there is nonetheless permanent damage to auditory nerve fiber (ANF) synapses with cochlear inner hair cells. Hidden hearing loss is a potential major health issue, as human temporal bone and ABR studies suggest it is common in humans. The remaining perceptual deficits in humans with clinically normal audiograms reflect temporal coding problems likely due to loss of the high threshold, low spontaneous rate ANFs, which are preferentially affected after TTS. The primary central targets of high-threshold ANFs reside in the small cell cap (SCC) of the cochlear nucleus (CN). High-threshold ANFs and their SCC targets display large dynamic ranges and superior suprathreshold tuning and temporal coding, which are essential for speech perception in noisy environments. The SCC occupies a large proportion of the CN in humans and is therefore poised to play a major role in central mechanisms of hidden hearing loss. The SCC is unique also as a putative recipient and projection area of medial olivocochlear (MOC) neurons. The overall hypothesis of this proposal is that the SCC plays a major role in suprathreshold sound coding and that this coding is highly susceptible to degradation by hidden hearing loss. The goal of this series of studies is to elucidate the cochlea- SCC-MOC circuit in normal and noise-damaged animals with hidden hearing loss, using state-of-the-art optogenetics, multichannel single unit physiology, tract tracing and sophisticated immunohistochemical methods.
'Hidden hearing loss' in which listeners with clinically normal audiograms still have difficulty understanding speech in noisy environments, is a potential major health issue, as human temporal bone and ABR studies suggest it is common in humans. The concept of hidden hearing loss challenges the view that hearing returns to normal after temporary threshold shift (TTS) following noise exposure. New evidence shows that while thresholds do indeed recover there is nonetheless permanent damage to the synapses between inner hair cells and auditory nerve fibers (ANF), in particular, those that are high threshold with low spontaneous rates. The effects of synaptopathy in hidden hearing loss have not been assessed on their central targets in the cochlear nucleus (CN). The high threshold ANFs project preferentially to the small cell cap region (SCC) of the CN, which also receives input from the medial olivocochlear (MOC) efferent system. The overall hypothesis of this proposal is that the SCC plays a major role in suprathreshold sound coding necessary for speech perception and that this coding is highly susceptible to degradation by hidden hearing loss. The goal of this series of studies is to elucidate the cochlea-SCC-MOC circuit in normal and noise- damaged animals with hidden hearing loss, using state-of-the-art optogenetics, physiology and tract tracing.
| Heeringa, Amarins N; Wu, Calvin; Chung, Christopher et al. (2018) Glutamatergic Projections to the Cochlear Nucleus are Redistributed in Tinnitus. Neuroscience 391:91-103 |
