The Stiffness Change of Conditioning Effect in Inner Hair Cells

过度暴露于强烈的声音会损害内耳细胞，导致永久性阈值移位（PTS）。调理作用可以保护耳朵免受听觉损伤。这种条件作用的机制尚不清楚。本课题通过原子力显微镜刚度测量，共聚焦显微镜f-actin和prestin的组织学观察，DPOAE电生理测定，阐明了调节作用的机制。本实验采用CBA品系小鼠。热应激（41.5度，15min）后3.6小时，外毛细胞的硬度升高。此外，在热应激后的12小时内，f-肌动蛋白也有所升高。另一方面，热应激后，外毛细胞中的特异性运动蛋白prestin没有升高。热应激后3 ~ 6 h， dpoae的输入输出函数增强。热应激-创伤间隔6小时，PTS得到显著保护。这些结果将揭示f-肌动蛋白通过改变内毛细胞的硬度而产生调节作用的机制。

Overexposure to intense sound damages the inner ear cells can lead to permanent threshold shift (PTS). Conditioning effect can protect the ear from acoustic injury. The mechanism of this conditioning effect has been still unknown.In this research project, the mechanism of conditioning effect has been clarified by using 1) stiffness measurement by atomic force microscopy, 2) histological findings of f-actin and prestin by confocal microscope, 3) electrophysiological assay by DPOAE measurement. CBA strain mice were used in this project. The stiffness of outer hair cells has been elevated at 3, 6 hours after heat stress (41.5 degree, 15min). Furthermore, f-actin also has been elevated for 12 hours after heat stress. On the other hand, prestin which is the specific motor protein in outer hair cells, has not been elevated after heat stress. The enhancement of DPOAEs input-output function were observed in the same time, 3 to 6 hours after heat stress. PTS was protected dramatically at 6hours heat stress-trauma interval. These results would show the mechanism of conditioning effect by changing the stiffness with f-actin in inner hair cells.