Effect of aging and noise on auditory function and oxidative changes in central and peripheral auditory system

• Main Authors: Jiun-Jen Huang, 黃俊仁
• Other Authors: Pei-Hsin Liu
• Format: Others
• Language: zh-TW
• Online Access: http://ndltd.ncl.edu.tw/handle/31556872200581056284

碩士 === 慈濟大學 === 神經科學研究所 === 96 === Recent studies revealed that reactive oxygen species (ROS) and reactive nitrogen species (RNS) play a significant role in cochlear pathologies induced by aging or noise. However, little is known about their effect on the central auditory system. Additionally, the conditions and the mechanisms under which noise-induced hearing loss (NIHL) and age-related hearing loss (ARHL) interact remain unknown. Male SD rats were divided into four groups: young rats (Y; 1 month old), young rats with noise exposure (YN; 8 kHz noise band at 120 dB sound pressure level for 2h), old rats (O; 1 year old), and old rats with noise exposure (ON). When evaluated by analysis of auditory brainstem response (ABR) 2 weeks after exposure, we found that compared to Y rats (control), threshold shifts of YN and ON rats significantly increased (p<0.05). Two months after exposure, the values of YN rats still maintained at a high level (18.81 ± 3.20 dB), however, that of ON rats apparently reduced (9.17 ± 1.44 dB). Regarding to central auditory system, noise induced oxidative damage evidenced by 3-nitrotyrosine (NT) labeling in superior olive (SPO) and cochlear nucleus (CN) of old but not young rats at 2 months postexposure. In contrast, noise induced oxidative damage in cochlear tissue of young but not old rats, including spiral ganglion neuron (SGN), spiral ligament (LIG), inner phalangeal cell (IPHC), and inner hair cell (IHC) at the same postexposure time. These results suggest that after noise exposure, old rats restore their hearing thresholds more rapidly than young rats. In addition, aging and noise-induced oxidative changes are present not only in peripheral but also central auditory tissues and these may play an important role in modulating NIHL and ARHL interactions.