Involvement of nitric oxide generation in noise-induced temporary threshold shift in guinea pigs

• Published in: Hearing research 2005-05, Vol.203 (1), p.94-100
• Main Authors: Chen, Yuh-Shyang, Tseng, Fen-Yu, Liu, Tien-Chen, Lin-Shiau, Shoei Yn, Hsu, Chuan-Jen
• Format: Article
• Language: English
• Subjects: Animals; Auditory Threshold; Biological and medical sciences; Ear and associated structures. Auditory pathways and centers. Hearing. Vocal organ. Phonation. Sound production. Echolocation; Ear, auditive nerve, cochleovestibular tract, facial nerve: diseases, semeiology; Evoked Potentials, Auditory, Brain Stem; Fundamental and applied biological sciences. Psychology; Guinea Pigs; Hearing Loss, Noise-Induced - metabolism; Hearing Loss, Noise-Induced - physiopathology; Male; Medical sciences; Nitric oxide; Nitric Oxide - biosynthesis; Nitric Oxide - metabolism; Noise; Non tumoral diseases; Osmolar Concentration; Otorhinolaryngology. Stomatology; Temporary threshold shift; Time Factors; Vertebrates: nervous system and sense organs
• ISSN: 0378-5955; 1878-5891
• DOI: 10.1016/j.heares.2004.12.006

The present study explored the role of endogenous nitric oxide (NO) in the temporary threshold shift caused by acoustic trauma. Guinea pigs were exposed to broadband white noise at a level of 105 ± 2 dB sound pressure level (SPL) for 10 min, causing a temporary threshold shift (TTS). The guinea pigs were divided into six groups (N-1 to N-6) according to survival days after noise exposure (0, 1, 2, 3, 7, 28 days). Auditory brainstem responses (ABR) were recorded before noise exposure, immediately after noise exposure and before sacrifice. Immediately after animals were sacrificed, the stria vascularis and the spiral ligament of the lateral wall of each individual cochlea were harvest as a unit and prepared for assay of NO. There was a significant correlation ( P < 0.001) between the NO concentration and final ABR threshold in the noise exposure groups. But the return of ABR threshold to pre-noise-exposed level is early than that of NO concentration. An average 16.2 dB threshold shift was found immediately after noise exposure. The threshold returned to the pre-noise-exposed level on the second post-exposure day. Comparing to unexposed control animals, the NO concentration increased nearly threefold immediately following noise exposure and decreased to twofold when the hearing threshold had returned to the pre-noise-exposed level. On the seventh post-exposure day the NO concentration was not different from that in unexposed control animals. Those findings indicate that endogenous NO is generated in the noise-induced temporal threshold shift and its concentration is correlated with the hearing loss.