title: Evaluating the protective role of the olivocochlear bundle against acoustic overexposure in rats by using Fos immunohistochemistry.
abstract: Efferent inhibition on the cochlea is suggested as a possible function of the olivocochlear bundle (OCB). Substantial evidence supports the finding that the OCB may protect the inner ear from noise-induced damage. However, there is relatively less known about the effects of noise on the central auditory transmission compared to the effects on the periphery. In the present animal study, two experimental paradigms were designed to analyze the influence of OCB lesion on the central auditory transmission following acoustic overexposure. In order to evaluate the animal's auditory function, its hearing threshold and the tone-evoked Fos expression shown in auditory nuclei were examined. Fos is a protein product of proto-oncogene c-fos. Via appropriate acoustic stimulation, Fos expression reveals the activated neuronal elements along the ascending auditory pathway. Thus, in experiment 1, no exposure sound was introduced and therefore no significant differences were shown in hearing thresholds and Fos expression among all rats, regardless of the status of their OCB. This result indicates that, without acoustic overexposure, OCB lesion caused no significant effect on brainstem auditory transmission. In contrast, in experiment 2, rats were exposed to continuous 8 kHz tones at 85 dB sound pressure level (SPL). A significantly increasing threshold was observed in rats with OCB lesion following an exposure period of 5 or 10 days. In addition, Fos expression was invisible first in rats with OCB lesion following 5-day exposure and almost no Fos expression could be examined in all rats after 10-day exposure. Taken together, the present data demonstrate that damaging the OCB renders an animal more easily vulnerable to acoustic damage than that of rat with intact OCB, and then reduces its cochlear activities, which eventually leads to increasing difficulty to induce tone-evoked Fos expression along the ascending auditory pathway.
authors.affiliation: Department of Physiology, Kaohsiung Medical University, Shih-Chuan 1st Road, 807, Kaohsiung, Taiwan. tsanju@cc.kmu.edu
authors.forename: T J
authors.initials: TJ
authors.lastname: Chen
authors.forename: S S
authors.initials: SS
authors.lastname: Chen
authors.forename: Y L
authors.initials: YL
authors.lastname: Hsieh
mesh_terms: D000818:Animals; D001306:Auditory Pathways / Q000378:metabolism / Q000503:physiopathology; D003051:Cochlea / Q000378:metabolism / Q000503:physiopathology*; D016057:Evoked Potentials, Auditory, Brain Stem / Q000502:physiology; D006317:Hearing Loss, Noise-Induced / Q000378:metabolism / Q000503:physiopathology*; D007150:Immunohistochemistry; D007245:Inferior Colliculi / Q000503:physiopathology; D008297:Male; D009847:Olivary Nucleus / Q000378:metabolism / Q000503:physiopathology*; D016761:Oncogene Proteins v-fos / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D016761:Oncogene Proteins v-fos