Heat stress and protection from permanent acoustic injury in mice

The inner ear can be permanently damaged by overexposure to high-level nois e; however, damage can be decreased by previous exposure to moderate level, nontraumatic noise (Canlon et al., 1988). The mechanism of this "protectiv e" 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 h eat stress in the ear. For physiological experiments, CBA/CaJ mice were exp osed 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 degrees C for 15 min). The interval between heat stress and sound e xposure varied in different groups from 6 to 96 hr. One week later, inner e ar function was assessed in each animal via comparison of compound action p otential thresholds to mean values from unexposed controls. Permanent thres hold shifts (PTSs) were similar to 40 dB in the group sound-exposed without previous heat stress. Heat-stressed animals were protected from acoustic i njury: mean PTS in the group with 6 hr heat-stress-trauma interval was redu ced to similar to 10 dB. This heat stress protection disappeared when the t reatment-trauma interval surpassed 24 hr. A parallel set of quantitative PC R experiments measured heat-shock protein mRNA in the cochlea and showed 10 0- to 200-fold increase over control 30 min after heat treatment, with leve ls returning to baseline at 6 hr after treatment. Results are consistent wi th the idea that upregulation of heat shock proteins protects the ear from acoustic injury.