Susan Shore: Cochlear damage may be necessary but not sufficient to induce tinnitus

New research from Susan Shore presented at last month’s 4th International Hearing Loss Conference…

Cochlear damage may be necessary but not sufficient to induce tinnitus

While hearing loss is associated with tinnitus, the relationship is not causal as people without audiometric hearing loss can develop tinnitus and not all people with audiometric hearing loss develop tinnitus.

Likewise, in animal models, noise exposures that produce only temporary threshold shifts result in behavioral evidence of tinnitus only in about half of the exposed animals. Following tinnitus-induction using narrow band noise exposures, we have demonstrated that dorsal cochlear nucleus fusiform cells show BF-specific alterations in stimulus-timing dependent plasticity, increased spontaneous synchronization, and increased spontaneous firing rates (SFR) in animals with behavioral evidence of tinnitus [1, 2].

Conversely, animals without plasticity-induced changes in fusiform cells, but equivalent degrees of cochlear damage, did not show evidence of tinnitus. Similarly, bushy cells in ventral cochlear nucleus showed BF-restricted increased SFR and cross-unit synchrony in animals with behavioral evidence of tinnitus but not in those without such behavioral evidence, even though ABR thresholds and suprathreshold wave-1 amplitudes were equivalent [3], suggesting similar cochlear damage in the two groups. Changes in glutamatergic and cholinergic transmission were also changed in these animals in a tinnitus-specific manner [4, 5].

Conclusions: These results suggest that hearing loss, whether visible or ‘hidden’, is insufficient by itself to produce a tinnitus phenotype. Changes in cochlear output after noise exposure require accompanying plastic changes in recipient neurons in the CNS in order to result in the physiological and behavioral signatures of tinnitus.

References: [1] C. Wu, D.T. Martel, S.E. Shore, Increased Synchrony and Bursting of Dorsal Cochlear Nucleus Fusiform Cells Correlate with Tinnitus, J Neurosci, 36 (2016) 2068-2073. [2] K.L. Marks, D.T. Martel, C. Wu, G.J. Basura, L.E. Roberts, K.C. Schvartz-Leyzac, S.E. Shore, Auditory-somatosensory bimodal stimulation desynchronizes brain circuitry to reduce tinnitus in guinea pigs and humans, Sci Transl Med, 10 (2018). [3] D. Martel, S. Shore, Ventral cochlear nucleus bushy cells contribute to enhanced auditory brainstem response amplitudes in tinnitus., ARO, 2019, DOI (2019). [4] A.N. Heeringa, C. Wu, C. Chung, M. West, D. Martel, L. Liberman, M.C. Liberman, S.E. Shore, Glutamatergic Projections to the Cochlear Nucleus are Redistributed in Tinnitus, Neuroscience, DOI 10.1016/j.neuroscience.2018.09.008(2018). [5] L. Zhang, C. Wu, D.T. Martel, M. West, M.A. Sutton, S.E. Shore, Remodeling of cholinergic input to the hippocampus after noise exposure and tinnitus induction in Guinea pigs, Hippocampus, DOI 10.1002/hipo.23058(2018).

SOURCE:

This information is from page 17 of the [PDF] International Hearing Loss Conference 2019 Program.


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