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The Journal of Neuroscience, November 15, 1999, 19(22):10116-10124

Heat Stress and Protection from Permanent Acoustic Injury in Mice

Naohiro Yoshida^{1, 2, 3}, Arthur Kristiansen^{1, 2}, and M. Charles Liberman^{1, 2}

¹ Eaton-Peabody Laboratory, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts 02114, ² Department of Otology and Laryngology, Harvard Medical School, Boston, Massachusetts 02114, and ³ Department of Otolaryngology, Tohoku University, Graduate School of Medicine, Sendai, 980-8574 Japan

The inner ear can be permanently damaged by overexposure to high-level noise; however, damage can be decreased by previous exposure to moderate level, nontraumatic noise (Canlon et al., 1988). The mechanism of this "protective" effect is unclear, but a role for heat shock proteins has been suggested. The aim of the present study was to directly test protective effects of heat stress in the ear. For physiological experiments, CBA/CaJ mice were exposed to an intense octave band of noise (8-16 kHz) at 100 dB SPL for 2 hr, either with or without previous whole-body heat stress (rectal temperature to 41.5 °C for 15 min). The interval between heat stress and sound exposure varied in different groups from 6 to 96 hr. One week later, inner ear function was assessed in each animal via comparison of compound action potential thresholds to mean values from unexposed controls. Permanent threshold shifts (PTSs) were ~40 dB in the group sound-exposed without previous heat stress. Heat-stressed animals were protected from acoustic injury: mean PTS in the group with 6 hr heat-stress-trauma interval was reduced to ~10 dB. This heat stress protection disappeared when the treatment-trauma interval surpassed 24 hr. A parallel set of quantitative PCR experiments measured heat-shock protein mRNA in the cochlea and showed 100- to 200-fold increase over control 30 min after heat treatment, with levels returning to baseline at 6 hr after treatment. Results are consistent with the idea that upregulation of heat shock proteins protects the ear from acoustic injury.

Key words: sound conditioning; acoustic trauma; cochlea; hearing; heat shock; quantitative PCR

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Copyright © 1999 Society for Neuroscience  0270-6474/99/192210116-09$05.00/0

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