Chen T J, Chen S S, Hsieh Y L
Department of Physiology, Kaohsiung Medical University, Shih-Chuan 1st Road, 807, Kaohsiung, Taiwan.
J Neurol Sci. 2000 Aug 15;177(2):104-13. doi: 10.1016/s0022-510x(00)00346-4.
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.
传出神经对耳蜗的抑制作用被认为是橄榄耳蜗束（OCB）的一种可能功能。大量证据支持OCB可能保护内耳免受噪声诱导损伤这一发现。然而，与噪声对周围听觉系统的影响相比，关于噪声对中枢听觉传导的影响相对了解较少。在本动物研究中，设计了两种实验范式来分析OCB损伤对声学过度暴露后中枢听觉传导的影响。为了评估动物的听觉功能，检测了其听力阈值以及听觉核团中音调诱发的Fos表达。Fos是原癌基因c-fos的蛋白质产物。通过适当的声学刺激，Fos表达揭示了沿听觉上行通路激活的神经元成分。因此，在实验1中，未引入暴露声音，所以无论OCB状态如何，所有大鼠的听力阈值和Fos表达均未显示出显著差异。该结果表明，在没有声学过度暴露的情况下，OCB损伤对脑干听觉传导没有显著影响。相比之下，在实验2中，大鼠暴露于85分贝声压级（SPL）的连续8千赫兹音调下。在暴露5天或10天后，OCB损伤的大鼠观察到阈值显著升高。此外，在暴露5天后，OCB损伤的大鼠中首先观察不到Fos表达，在暴露10天后，所有大鼠几乎都检测不到Fos表达。综上所述，目前的数据表明，与OCB完整的大鼠相比，损伤OCB使动物更容易受到声学损伤，进而降低其耳蜗活动，最终导致沿听觉上行通路诱发音调诱发Fos表达的难度增加。
