Abstract
Objective: The steroid drugs are used for the standard treatment of sudden sensorineural hearing loss. However, clinical results on the effect of glucocorticoids in acoustic trauma have not yet been understood well. The effects of glucocorticoid receptor (GR) antagonist, mifepristone, on the cochlea sensitivity loss due to short-term sound exposure were studied in the guinea pig. Methods: Mifepristone (20 mg/kg) was injected subcutaneously immediately after the noise exposure to 4 kHz pure tone of 100 or 120 dB SPL for 10 min and also at 1 day and 3 days later. Seven days after the sound exposure, the compound action potentials (CAPs) of the cochlear nerve and the 2f1–f2 distortion product oto-acoustic emissions (DPOAEs) were recorded. Results: No significant CAP threshold losses were observed in either mifepristone or saline administration after the exposure at 100 dB SPL. After the exposure at 120 dB SPL, administration of mifepristone elevated the CAP threshold at 5–8 kHz significantly as compared with the saline administration. The DPOAE output shifts of both saline and mifepristone groups were similar to each other. Conclusion: Mifepristone may influence inner hair cells (IHCs) and afferent nerve fibers beneath the IHC without having influence on outer hair cells (OHCs). It is suggested that glucocorticoid plays an important role in the improvement of hearing impairment after loud sound exposure.
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