PT  - JOURNAL ARTICLE
AU  - Naohiro Yoshida
AU  - Arthur Kristiansen
AU  - M. Charles Liberman
TI  - Heat Stress and Protection from Permanent Acoustic Injury in Mice
AID  - 10.1523/JNEUROSCI.19-22-10116.1999
DP  - 1999 Nov 15
TA  - The Journal of Neuroscience
PG  - 10116--10124
VI  - 19
IP  - 22
4099  - http://www.jneurosci.org/content/19/22/10116.short
4100  - http://www.jneurosci.org/content/19/22/10116.full
SO  - J. Neurosci.1999 Nov 15; 19
AB  - 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.