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The Journal of Neuroscience, February 15, 2006, 26(7):2115-2123; doi:10.1523/JNEUROSCI.4985-05.2006

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Behavioral/Systems/Cognitive
Acceleration of Age-Related Hearing Loss by Early Noise Exposure: Evidence of a Misspent Youth

Sharon G. Kujawa^1,2,3,4 and M. Charles Liberman^1,3,4

¹Eaton-Peabody Laboratory and ²Department of Audiology, Massachusetts Eye and Ear Infirmary, and ³Department of Otology and Laryngology, Harvard Medical School, Boston, Massachusetts 02114, and ⁴Division of Health Science and Technology, Harvard University/Massachusetts Institute of Technology, Boston, Massachusetts 02139

Correspondence should be addressed to Dr. Sharon G. Kujawa, Massachusetts Eye and Ear Infirmary, 243 Charles Street, Boston, MA 02114-3096. Email: sharon_kujawa{at}meei.harvard.edu

Age-related and noise-induced hearing losses in humans are multifactorial, with contributions from, and potential interactions among, numerous variables that can shape final outcome. A recent retrospective clinical study suggests an age–noise interaction that exacerbates age-related hearing loss in previously noise-damaged ears (Gates et al., 2000). Here, we address the issue in an animal model by comparing noise-induced and age-related hearing loss (NIHL; AHL) in groups of CBA/CaJ mice exposed identically (8–16 kHz noise band at 100 dB sound pressure level for 2 h) but at different ages (4–124 weeks) and held with unexposed cohorts for different postexposure times (2–96 weeks). When evaluated 2 weeks after exposure, maximum threshold shifts in young-exposed animals (4–8 weeks) were 40–50 dB; older-exposed animals (16 weeks) showed essentially no shift at the same postexposure time. However, when held for long postexposure times, animals with previous exposure demonstrated AHL and histopathology fundamentally unlike unexposed, aging animals or old-exposed animals held for 2 weeks only. Specifically, they showed substantial, ongoing deterioration of cochlear neural responses, without additional change in preneural responses, and corresponding histologic evidence of primary neural degeneration throughout the cochlea. This was true particularly for young-exposed animals; however, delayed neuropathy was observed in all noise-exposed animals held 96 weeks after exposure, even those that showed no NIHL 2 weeks after exposure. Data suggest that pathologic but sublethal changes initiated by early noise exposure render the inner ears significantly more vulnerable to aging.

Key words: mouse; noise-induced hearing loss; age-related hearing loss; primary neural degeneration; neuropathy; auditory

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Received Nov. 22, 2005; revised Jan. 6, 2006; accepted Jan. 11, 2006.

Correspondence should be addressed to Dr. Sharon G. Kujawa, Massachusetts Eye and Ear Infirmary, 243 Charles Street, Boston, MA 02114-3096. Email: sharon_kujawa{at}meei.harvard.edu

This article has been cited by other articles:

				S. G. Kujawa and M. C. Liberman Adding Insult to Injury: Cochlear Nerve Degeneration after "Temporary" Noise-Induced Hearing Loss J. Neurosci., November 11, 2009; 29(45): 14077 - 14085. [Abstract] [Full Text] [PDF]

				Z. Chen, M. Peppi, S. G. Kujawa, and W. F. Sewell Regulated Expression of Surface AMPA Receptors Reduces Excitotoxicity in Auditory Neurons J Neurophysiol, August 1, 2009; 102(2): 1152 - 1159. [Abstract] [Full Text] [PDF]

				A. E. Holmes, S. E. Widen, S. Erlandsson, C. L. Carver, and L. L. White Perceived Hearing Status and Attitudes Toward Noise in Young Adults Am J Audiol, December 1, 2007; 16(2): S182 - S189. [Abstract] [Full Text] [PDF]

				X. Liu, O. V. Bulgakov, K. N. Darrow, B. Pawlyk, M. Adamian, M. C. Liberman, and T. Li Usherin is required for maintenance of retinal photoreceptors and normal development of cochlear hair cells PNAS, March 13, 2007; 104(11): 4413 - 4418. [Abstract] [Full Text] [PDF]

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