Effects of heat stress on Young's modulus of outer hair cells in mice
Effects of heat stress on Young's modulus of outer hair cells in mice
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DOI：
10.1016/j.brainres.2006.05.095
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发表时间：
2006-08
期刊：
影响因子：
2.9
通讯作者：
M. Murakoshi;N. Yoshida;Y. Kitsunai;Koji Iida;S. Kumano;Takashi Suzuki;Toshimitsu Kobayashi;H. Wada
中科院分区：
文献类型：
--
作者：
M. Murakoshi;N. Yoshida;Y. Kitsunai;Koji Iida;S. Kumano;Takashi Suzuki;Toshimitsu Kobayashi;H. Wada
强烈的声音暴露会导致永久性听力损失，由于毛细胞和耳蜗损伤。预先使用亚致死性应激源，如非创伤性声音、热应激和约束，可以保护耳朵免受声损伤。然而，条件反射相关的耳蜗保护机制仍然未知。本文采用原子力显微镜和激光共聚焦显微镜分别研究了热应激前后外毛细胞（OHCs）的杨氏模量和丝状肌动蛋白（F-actin）的变化。在3-6 h时，OHCs的杨氏模量随热应力的增加而显著增加，到12 h时开始下降，48 h时恢复到热应力处理前的水平。F-actin含量在热应激后3 h开始增加，12 h达到高峰。热应激后24 h开始下降，48-96 h恢复到预处理水平。这些时间过程与先前的报告一致，其中热应激显示出抑制永久性阈值偏移（PTS）。此外，畸变产物耳声发射（DPOAE）被证实是由热应力增强。这些结果表明，空调与热应力在结构上修改OHC，使他们变得僵硬，由于增加的F-肌动蛋白的量。因此，当OHC暴露在大噪音中时，它们可能会经历更少的压力，从而保护哺乳动物的听力免受创伤性噪音的影响。
Intense sound exposure causes permanent hearing loss due to hair cell and cochlear damage. Prior conditioning with sublethal stressors, such as nontraumatic sound, heat stress and restraint protects the ear from acoustic injury. However, the mechanisms underlying conditioning-related cochlear protection remain unknown. In this paper, Young's modulus and the amount of filamentous actin (F-actin) of outer hair cells (OHCs) with/without heat stress were investigated by atomic force microscopy and confocal laser scanning microscopy, respectively. Conditioning with heat stress resulted in a statistically significant increase in Young's modulus of OHCs at 3–6 h after application, and such modulus then began to decrease by 12 h and returned to pre-conditioning level at 48 h after heat stress. The amount of F-actin began to increase by 3 h after heat stress and peaked at 12 h. It then began to decrease by 24 h and returned to the pre-conditioning level by 48–96 h after heat stress. These time courses are consistent with a previous report in which heat stress was shown to suppress permanent threshold shift (PTS). In addition, distortion product otoacoustic emissions (DPOAEs) were confirmed to be enhanced by heat stress. These results suggest that conditioning with heat stress structurally modifies OHCs so that they become stiffer due to an increase in the amount of F-actin. As a consequence, OHCs possibly experience less strain when they are exposed to loud noise, resulting in protection of mammalian hearing from traumatic noise exposure.