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Semin Hear 2003; 24(2): 111-114
DOI: 10.1055/s-2003-39837
Copyright © 2002 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.: +1(212) 584-4662

Progression of Outer Hair Cell Death in the Chinchilla Cochlea following Traumatic Noise Exposure

Bo Hua Hu1 , Donald Henderson1 , Thomas M. Nicotera2
  • 1Center for Hearing and Deafness, State University of New York at Buffalo, New York
  • 2Roswell Park Cancer Institute, Department of Molecular and Cellular Biophysics, Buffalo, New York
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Publication Date:
11 June 2003 (online)

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ABSTRACT

Permanent hearing loss by noise exposure is the functional consequence of a complex set of pathological changes in the cochlea. Among these changes, hair cell (HC) death may contribute most to the loss of auditory function. It has been known that noise-induced HC death starts during a noise exposure and continues even after the termination of the noise exposure. Biological mechanisms underlying the progression of HC death are not fully understood. Here we describe progression of HC death in the chinchilla cochlea after exposure to a 4-kHz narrow band noise at 110 dB sound pressure level (SPL) for 1 hour. Morphological examination of HC nuclei revealed typical nuclear changes for both apoptosis and necrosis. Apoptosis appeared to be a major death pathway leading to progression of the cochlear lesion in noise-damaged cochleas. The study also showed that expansion of HC death developed asymmetrically toward the apical and basal parts of the cochleas. Detection of caspase-3 activation showed a spatial agreement between the apoptotic nuclear changes and caspase-3 activation. These results clearly implicate the apoptotic pathway in the postexposure progression of HC demise.

KEYWORDS

Noise - hair cell - apoptosis - cochlea

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