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Ameliorative effects of an augmented acoustic environment on age-related hearing loss in middle-aged Fischer 344/NHsd rats

Authors

  • Chiemi Tanaka MA,

    Corresponding author
    1. Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, State University of New York at Buffalo, Buffalo, New York, U.S.A.
    • Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, State University of New York at Buffalo, 137 Cary Hall, 3435 Main Street, Buffalo, NY 14214, U.S.A.
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  • Eric C. Bielefeld PhD,

    1. Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, State University of New York at Buffalo, Buffalo, New York, U.S.A.
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  • Guang-Di Chen PhD,

    1. Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, State University of New York at Buffalo, Buffalo, New York, U.S.A.
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  • Manna Li MD, PhD,

    1. Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, State University of New York at Buffalo, Buffalo, New York, U.S.A.
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  • Donald Henderson PhD

    1. Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, State University of New York at Buffalo, Buffalo, New York, U.S.A.
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  • Presented at the 32nd Annual Mid-Winter Meeting of the Association for Research in Otolaryngology, Baltimore, Maryland, U.S.A., February, 2009.

Abstract

Objectives/Hypothesis:

To investigate the effects of an augmented acoustic environment (AAE) on age-related hearing loss (ARHL) and outer hair cell (OHC) pathology in middle-aged Fischer 344/NHsd (F344/NHsd) rats.

Methods:

Eleven F344/NHsd rats were divided into two groups: 1) the AAE group (n = 5), which was exposed to 4–20 kHz broadband noise at 80 dB SPL for 12 h/d, 5 d/wk for 13 weeks starting from 16 months of age; and 2) the control group (n = 6), which did not receive the AAE during the same time span. Auditory brainstem response thresholds were obtained at different time points, and OHC pathology was examined after 13 weeks of AAE using propidium iodide and antiprestin antibody staining.

Results:

The AAE-treated rats showed smaller mean threshold shifts (−1 to −3 dB) at 20–40 kHz than the control group (7.5–16.7 dB) at 13 weeks. No significant group differences were observed in the percentage of missing OHCs or abnormal OHC nuclei. However, examination of prestin in a pair of AAE and control rats revealed more uniform prestin staining intensity among OHCs in the AAE-treated cochlea than in the control cochlea.

Conclusions:

Thirteen-week AAE treatment in the middle-aged F344/NHsd rats slowed progression of ARHL. The AAE did not show a significant effect on OHC degeneration, but it is speculated that the AAE may maintain the integrity of prestin to preserve OHC functionality. However, further study is warranted to understand the protective mechanism of AAE as an intervention against ARHL. Laryngoscope, 2009

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