Heat Stress and Protection from Permanent Acoustic Injury in Mice
| Autor: | Arthur G. Kristiansen, Naohiro Yoshida, M. Charles Liberman |
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| Rok vydání: | 1999 |
| Předmět: |
Male
medicine.medical_specialty Hot Temperature Transcription Genetic Action Potentials Anesthesia General Body Temperature Mice Sound exposure Stress Physiological Internal medicine Heat shock protein otorhinolaryngologic diseases Animals Medicine Inner ear RNA Messenger ARTICLE Heat-Shock Proteins Cochlea business.industry General Neuroscience Auditory Threshold Rectal temperature Compound muscle action potential Surgery Heat stress Endocrinology medicine.anatomical_structure Acoustic Stimulation Gene Expression Regulation Hearing Loss Noise-Induced Ear Inner Mice Inbred CBA Noise business After treatment |
| Zdroj: | The Journal of Neuroscience. 19:10116-10124 |
| ISSN: | 1529-2401 0270-6474 |
| DOI: | 10.1523/jneurosci.19-22-10116.1999 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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