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Front. Syst. Neurosci. | doi: 10.3389/fnsys.2018.00059

Cochlear synaptopathy changes sound-evoked activity without changing spontaneous discharge in the mouse inferior colliculus

  • 1Oregon Hearing Research Center, Oregon Health & Science University, United States
  • 2Department of Otolaryngology, Harvard Medical School, United States
  • 3Massachusetts Eye & Ear Infirmary, Harvard Medical School, United States

Tinnitus and hyperacusis are life-disrupting perceptual abnormalities that are often preceded by acoustic overexposure. Animal models of overexposure have suggested a link between these phenomena and neural hyperactivity, i.e. elevated spontaneous rates (SRs) and sound-evoked responses. Prior work has focused on changes in central auditory responses, with less attention paid to the exact nature of the associated cochlear damage. The demonstration that acoustic overexposure can cause cochlear neuropathy without permanent threshold elevation suggests cochlear neuropathy per se may be a key elicitor of neural hyperactivity. We addressed this hypothesis by recording responses in the mouse inferior colliculus (IC) following a bilateral, neuropathic noise exposure. One to three wks post-exposure, mean SRs were unchanged in mice recorded while awake, or under anesthesia. SRs were also unaffected by more intense, or unilateral exposures. These results suggest that neither neuropathy nor hair cell loss are sufficient to raise SRs in the IC, at least in 7-wk-old mice, one to three wks post exposure. However, it’s not clear whether our mice had tinnitus. Tone-evoked rate-level functions at the CF were steeper following exposure, specifically in the region of maximal neuropathy. Furthermore, suppression driven by off-CF tones and by ipsilateral noise were also reduced. Both changes were especially pronounced in neurons of awake mice. This neural hypersensitivity may manifest as behavioral hypersensitivity to sound - prior work reports that this same exposure causes elevated acoustic startle. Together, these results indicate that neuropathy may initiate a compensatory response in the central auditory system leading to the genesis of hyperacusis.

Keywords: cochlear synaptopathy, Tinnitus, Hyperacusis, noise exposure, inferior colliculus

Received: 04 Sep 2018; Accepted: 26 Oct 2018.

Edited by:

Preston E. Garraghty, Indiana University Bloomington, United States

Reviewed by:

Todd M. Mowery, New York University, United States
Andrej Kral, Hannover Medical School, Germany  

Copyright: © 2018 Shaheen and Liberman. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: PhD. Luke A. Shaheen, Oregon Health & Science University, Oregon Hearing Research Center, Portland, 97239, Oregon, United States, shaheenl@ohsu.edu