{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T15:35:10Z","timestamp":1791473710583,"version":"4.3.4"},"reference-count":72,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[2014,2,1]]},"abstract":"<jats:p>Perceptual abnormalities such as hyperacusis and tinnitus often occur after acoustic overexposure. Although such exposure can also result in permanent threshold elevation, some individuals with noise-induced hyperacusis or tinnitus show clinically normal thresholds. Recent work in animals has shown that a \u201cneuropathic\u201d noise exposure can cause immediate, permanent degeneration of the cochlear nerve despite complete threshold recovery and lack of hair cell damage (Kujawa SG, Liberman MC. J Neurosci 29: 14077\u201314085, 2009; Lin HW, Furman AC, Kujawa SG, Liberman MC. J Assoc Res Otolaryngol 12: 605\u2013616, 2011). Here we ask whether this noise-induced primary neuronal degeneration results in abnormal auditory behavior, based on the acoustic startle response (ASR) and prepulse inhibition (PPI) of startle. Responses were measured in mice exposed either to a \u201cneuropathic\u201d noise or to a lower-intensity, \u201cnonneuropathic\u201d noise and in unexposed control mice. Mice with cochlear neuropathy displayed hyperresponsivity to sound, evidenced by enhanced ASR and PPI, while exposed mice without neuronal loss showed controllike responses. Gap PPI tests, often used to assess tinnitus, revealed limited gap detection deficits in mice with cochlear neuropathy only for certain gap-startle latencies, inconsistent with the presence of tinnitus \u201cfilling in the gap.\u201d Despite significantly reduced wave 1 of the auditory brainstem response, representing cochlear nerve activity, later peaks were unchanged or enhanced, suggesting compensatory neural hyperactivity in the auditory brainstem. Considering the rapid postexposure onset of both cochlear neuropathy and exaggerated startle-based behavior, the results suggest a role for cochlear primary neuronal degeneration, per se, in the central neural excitability that could underlie the generation of hyperacusis.<\/jats:p>","DOI":"10.1152\/jn.00184.2013","type":"journal-article","created":{"date-parts":[[2013,11,7]],"date-time":"2013-11-07T03:59:58Z","timestamp":1383796798000},"page":"552-564","source":"Crossref","is-referenced-by-count":289,"title":["Is noise-induced cochlear neuropathy key to the generation of hyperacusis or tinnitus?"],"prefix":"10.1152","volume":"111","author":[{"given":"Ann E.","family":"Hickox","sequence":"first","affiliation":[{"name":"Program in Speech and Hearing Bioscience and Technology, Harvard-MIT Division of Health Sciences and Technology, Cambridge, Massachusetts;"},{"name":"Eaton-Peabody Laboratory, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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