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Relationship between Tinnitus and IHC synaptopathy in an animal model
18 April 2018 (online)
Hearing loss is often accompanied by comorbidities like tinnitus, a phantom perception of sound which in western civilizations affects up to 15% of the adult population. As studies in rodents could show, tinnitus may not only be a result of hearing loss due to cochlear hair cell damage but can also be a consequence of synaptopathy at the inner hair cells (IHC) already induced by moderate sound traumata (hidden hearing loss, HHL).
Here we investigate the IHC synaptopathy in our animal model, the Mongolian gerbil, and relate it to behavioral signs of tinnitus in this species. Tinnitus was induced by a mild monaural acoustic trauma which in > 90% of the animals leads to a monaural noise induced hearing loss in the animals, as quantified by brainstem response audiometry. Behavioral signs of tinnitus percepts were detected by GPIAS (gap pre-pulse inhibition of the acoustic startle response) in about two-thirds of the animals. 14 days after trauma the cochleae of traumatized and non-traumatized ears were isolated and inner hair cell synapses were counted within several spectral regions of the cochlea.
Inner hair cell synaptopathy was only found in animals with behavioral signs of tinnitus, independent of type of hearing loss (HHL or threshold increase). On the other hand, animals with apparent hearing loss but without behavioral signs of tinnitus showed a reduction in amplitudes of auditory brainstem response waves I/II (cochlear nerve and dorsal cochlear nucleus) but no significant changes in the number of synapses at the inner hair cells.
We conclude – in line with the literature – that hearing loss is caused by damage to the inner and/or outer hair cells, but that the development of tinnitus, at least in our animal model, is closely linked to synaptopathy at the IHC.
No conflict of interest has been declared by the author(s).