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Updated: Jul 7, 2026

Modified Experimental Conditions for Noise-Induced Hearing Loss in Mice and Assessment of Hearing Function and Outer Hair Cell Damage
Published on: February 10, 2023
Chronologic changes of nitric oxide concentration in the cochlear lateral wall and its role in noise-induced
Yuh-Shyang Chen1, Fen-Yu Tseng, Kai-Nan Lin
1Department of Otolaryngology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Objective:
The objective of this study was to investigate the chronologic changes of nitric oxide (NO) concentration in the cochlear lateral wall and to explore its possible role in permanent threshold shift (PTS) after intense noise exposure.
Materials And Methods:
Seventeen guinea pigs were subjected to a single continuous exposure to broadband white noise at 105 +/- 2 dB sound pressure level (SPL) for 40 hours and were divided into four groups according to various postnoise recovery periods. Another 12 guinea pigs were not exposed to noise and served as controls. The hearing status of all animals was evaluated with auditory brainstem responses (ABR) evoked by condensation "click" sounds. ABR were recorded both prior to noise exposure and immediately before killing the animal. After death, NO concentration in the cochlear lateral wall was directly measured with an NO/ozone chemiluminescence technique.
Results:
An approximately 1.7-fold increase in NO concentration was observed immediately postnoise exposure, which persisted for up to 28 days. The threshold of ABR elevation (mean, 30 dB SPL) peaked immediately after cessation of noise exposure and gradually resolved to a PTS (mean, 14.5 dB SPL) 56 days after noise exposure when NO concentration had returned to its prenoise exposure level.
Conclusion:
Noise-induced threshold shift, which resolved to a mild PTS, can be partially attributed to NO elevation in the cochlear lateral wall. Our results revealed a nonlinear correlation between ABR recovery and depletion of NO, indicating that the mechanisms of NO changes in the cochlear lateral wall may be more complicated than previously conceived and that other pathophysiologic mechanisms may also play important roles in noise-induced PTS.
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