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Effects of cochlear synaptopathy on spontaneous and sound-evoked activity in the mouse inferior colliculus

Luke A. Shaheen, View ORCID ProfileM. Charles Liberman
doi: https://doi.org/10.1101/381087
Luke A. Shaheen
1Oregon Hearing Research Center, Oregon Health &Science University, Portland OR, USA
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M. Charles Liberman
2Department of Otology and Laryngology, Harvard Medical School, Boston MA, USA
3Eaton-Peabody Laboratories, Massachusetts Eye &Ear Infirmary, Boston MA, USA
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  • ORCID record for M. Charles Liberman
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ABSTRACT

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 peripheral damage. The demonstration that acoustic overexposure can cause cochlear nerve damage without permanent threshold elevation suggests this type of peripheral damage may be a key elicitor of tinnitus and hyperacusis in humans with normal audiograms. We addressed this idea by recording responses in the mouse inferior colliculus (IC) following a bilateral, neuropathic noise exposure. Two 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 mice. 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. These findings align with prior reports of elevated acoustic startle in neuropathic mice, and indicate that neuropathy may initiate a compensatory response in the central auditory system leading to the genesis of hyperacusis.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted August 06, 2018.
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Effects of cochlear synaptopathy on spontaneous and sound-evoked activity in the mouse inferior colliculus
Luke A. Shaheen, M. Charles Liberman
bioRxiv 381087; doi: https://doi.org/10.1101/381087
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Effects of cochlear synaptopathy on spontaneous and sound-evoked activity in the mouse inferior colliculus
Luke A. Shaheen, M. Charles Liberman
bioRxiv 381087; doi: https://doi.org/10.1101/381087

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