The Stiffness Change of Conditioning Effect in Inner Hair Cells

对强声音的过度刺激会损伤内耳细胞，导致永久性听阈移（PTS）。条件反射效应可以保护耳朵免受声损伤。本研究通过原子力显微镜对骨骼肌的硬度测量、共聚焦显微镜对f-actin和普雷斯廷的组织学观察以及DPOAE对骨骼肌电生理的检测，对骨骼肌的条件反射作用机制进行了初步探讨。CBA品系小鼠用于本项目。热应激（41.5 ℃，15 min）后3、6 h，外毛细胞硬度升高。此外，f-肌动蛋白在热应激后12小时也有所升高。另一方面，普雷斯廷是外毛细胞中的特异性运动蛋白，在热应激后没有升高。热应激后3 ~ 6 h，DPOAEs输入输出功能增强。热应激-创伤间隔6 h时，PTS明显受到保护。这些结果将揭示内毛细胞中肌动蛋白改变刚度的调节作用机制。

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.