Abstract

Conclusion. After a noise-induced transient threshold shift, hypoxia occurred in the central nervous system, especially in the auditory cortex, the hippocampus, and the inferior colliculus. Objectives. Noise-induced inner ear hypoxia was shown by measurement of an increase in hypoxia-inducible factor-1 alpha, which is expressed? in the nucleus under hypoxic conditions. This study uses pimonidazole to localize site-specific hypoxic changes occurring in the mouse central auditory pathway during noise-induced auditory threshold shift. Method. BALB/c hybrid mice with normal hearing were exposed to 122 dB SPL white noise for 3 h. Immediately after exposure to the noise, and 7 d after noise exposure, the brains of mice were collected. Brains were cryosectioned into slices 15 µm thick and examined by immunofluorescence after staining with pimonidazole HCl. Results. After 3 h of exposure to 120 dB SPL noise, the hearing thresholds of mice decreased to 51.1±8.6 dB SPL (n =14), but hearing recovered in 7 d. After noise exposure, pimonidazole signal increased in the auditory cortex, the hippocampus, and the inferior colliculus. The pimonidazole signal remained elevated after 7 d. In control mice, pimonidazole did not stain any brain region.

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