Chen Guang-Di
Center for Hearing and Deafness, 137 Cary Hall, 3435 Main Street, SUNY at Buffalo, Buffalo, NY 14214, USA.
Hear Res. 2006 Dec;222(1-2):54-61. doi: 10.1016/j.heares.2006.08.011. Epub 2006 Sep 26.
Noise-induced permanent loss of cochlear amplification was observed previously with the majority of outer hair cells (OHCs) still surviving in the cochlea and even with a normal OHC receptor potential, indicated by CM (cochlear microphonics) recording [Chen, G.D., Fechter, L.D., 2003. The relationship between noise-induced hearing loss and hair cell loss in rats. Hear. Res. 177(1-2), 81-90; Chen, G.D., Liu, Y., 2005. Mechanisms of noise-induced hearing loss potentiation by hypoxia. Hear. Res. 200, 1-9]. This study focused on effects of an intense noise exposure (10-20 kHz at a level of 110 dB SPL for 4 h) on the OHC motor protein (prestin) and structural proteins in the OHC membrane skeleton. The noise exposure significantly disrupted CM and CAP (cochlear compound action potential). The injured CM recovered after 1-week resting period. The impaired CAP at frequencies lower than the noise band also recovered. However, the CAP recovery at frequencies of the noise band stopped at a linear line one week after the noise exposure, indicating a permanent loss of cochlear amplification. Gene expression of prestin, beta-spectrin, and beta-actin was significantly up-regulated after the noise exposure. The elevated gene expression peaked at the 3rd post-exposure day and returned to baseline 4 weeks after the noise exposure. The up-regulated gene expression may be in response to injury of the proteins, which may be responsible for the loss of cochlear amplification.
此前观察到，噪声引起的耳蜗放大功能永久性丧失时，耳蜗中的大多数外毛细胞（OHC）仍然存活，甚至通过耳蜗微音电位（CM）记录显示OHC受体电位正常[陈，G.D.，费克特，L.D.，2003年。大鼠噪声性听力损失与毛细胞损失之间的关系。听觉研究。177(1 - 2)，81 - 90；陈，G.D.，刘，Y.，2005年。缺氧增强噪声性听力损失的机制。听觉研究。200，1 - 9]。本研究聚焦于强烈噪声暴露（10 - 20千赫兹，110分贝声压级，持续4小时）对OHC运动蛋白（prestin）和OHC膜骨架结构蛋白的影响。噪声暴露显著破坏了CM和耳蜗复合动作电位（CAP）。休息1周后，受损的CM恢复。噪声频段以下频率的受损CAP也恢复。然而，噪声暴露1周后，噪声频段频率的CAP恢复停留在一条直线上，表明耳蜗放大功能永久性丧失。噪声暴露后，prestin、β - 血影蛋白和β - 肌动蛋白的基因表达显著上调。基因表达升高在暴露后第3天达到峰值，噪声暴露4周后恢复到基线水平。基因表达上调可能是对蛋白质损伤的反应，这可能是耳蜗放大功能丧失的原因。
