4.5 Article

Relationship between Auditory Thresholds, Central Spontaneous Activity, and Hair Cell Loss after Acoustic Trauma

期刊

JOURNAL OF COMPARATIVE NEUROLOGY
卷 519, 期 13, 页码 2637-2647

出版社

WILEY-BLACKWELL
DOI: 10.1002/cne.22644

关键词

tinnitus; inferior colliculus; guinea pig; cochleogram; compound action potential

资金

  1. Royal National Institute for Deaf People (UK) [G37]
  2. Medical Health and Research Infrastructure Fund (WA)
  3. University of Western Australia
  4. National Institutes of Health (NIH) [R01-DC009091, R01-DC009219-01]
  5. RNID [G55] Funding Source: researchfish

向作者/读者索取更多资源

Acoustic trauma caused by exposure to a very loud sound increases spontaneous activity in central auditory structures such as the inferior colliculus. This hyperactivity has been suggested as a neural substrate for tinnitus, a phantom hearing sensation. In previous studies we have described a tentative link between the frequency region of hearing impairment and the corresponding tonotopic regions in the inferior colliculus showing hyperactivity. In this study we further investigated the relationship between cochlear compound action potential threshold loss, cochlear outer and inner hair cell loss, and central hyperactivity in inferior colliculus of guinea pigs. Two weeks after a 10-kHz pure tone acoustic trauma, a tight relationship was demonstrated between the frequency region of compound action potential threshold loss and frequency regions in the inferior colliculus showing hyperactivity. Extending the duration of the acoustic trauma from 1 to 2 hours did not result in significant increases in final cochlear threshold loss, but did result in a further increase of spontaneous firing rates in the inferior colliculus. Interestingly, hair cell loss was not present in the frequency regions where elevated cochlear thresholds and central hyperactivity were measured, suggesting that subtle changes in hair cell or primary afferent neural function are sufficient for central hyperactivity to be triggered and maintained. J. Comp. Neurol. 519:2637-2647, 2011. (C) 2011 Wiley-Liss, Inc.

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