噪声暴露对豚鼠耳蜗内毛细胞下传入神经末梢的损伤

The damage of the afferent nerve endings underlying cochlear inner hair cells in guinea pigs caused by noise exposure

为了观察噪声暴露对耳蜗内毛细胞下传入神经末梢的损伤,探讨引起损伤的过量谷氨酸兴奋毒性机制,将实验动物随机分为正常对照组与噪声暴露后8小时、1天、3天和 7天组。正常对照组不给噪声;实验组暴露于 120 dB Lp及 1/3倍频程的 4 kHz窄带噪声中 4小时。测试噪声暴露前、后不同时间各组动物耳蜗微音器电位（Cochlear Microphonics,CM）幅度和听神经复合动作电位（Compound Action Potential,CAP）阈值;在透射电镜下观察噪声暴露后耳蜗形态学及内毛细胞中谷氨酸免疫金颗粒密度的变化。结果表明:（1）噪声暴露后,豚鼠CM非线性特性减弱,CAP阈值升高;外毛细胞胞浆和内毛细胞下传入神经末梢有空泡形成。随着噪声暴露后时间的延长,上述改变逐渐减轻,但当CM非线性特性与外毛细胞形态学变化基本恢复时,CAP仍有显著阈移,内毛细胞下传入神经末梢空泡仍存在。（2）内毛细胞中谷氨酸免疫金颗粒密度在噪声暴露后8小时降低,在噪声暴露后1天、3天和7天恢复。从而说明:（1）噪声暴露不仅损伤外毛细胞,而且损伤内毛细胞下传入神经末梢。（3）噪声暴露后内毛细胞传入神经递质谷氨酸过度释放引起内毛细胞下传入神经末梢的兴奋毒性损伤。

Objective To observe the damage of the afferent nerve endings underlying cochlear Inner Hair Cells (IHCs) caused by noise exposure, and to explore the injury mechanism of the above lesion with respect to the excitotoxicity of the excessive afferent neurotransmitter glutamate in cochlea. Methods Thirty-eight guinea pigs served as subjects. The animals were randomly distributed into 5 groups: a normal control group, and 4 experimental groups including the group of 8 hours, 1 day, 3 days and 7 days after noise exposure. The 4 experimental groups were immersed in the noise of 120 dB Lp, 1/3 octave 4 kHz narrow band noise for 4 h. The altitude of Cochlea Microphonics (CM) and the response threshold of Compound Action Potential (CAP) in the left ear of animals were measured. Ultrathin sections (70 nm) were cut from the Corti organs of the animals' left ear. The ultrastructural changes of cochlea and the densities of glutamateimmunogold particle in IHCs and Outer Hair Cells (OHCs) were observed under the transmission electron microscope. Results In the four experimental groups, the non-linear property of CM lessened and the threshold of CAP enhanced, and vacuolizations appeared in the cell plasma of OHCs and in the afferent nerve endings underneath IHCs. Compared with that of the normal control group, the immunogold particle densities of IHCs in the left ear reduced significantly at the group of 8 hours after noise exposure, but there were no significant difference in the group of 1 day, 3 days and 7 days after noise exposure respectively. Conclusion (1) The damaged portion of cochlea caused by noise exposure not only involves OHCs, but also the afferent nerve endings underneath IHCs; (2) The afferent neurotransmitter glutamate in IHCs can be over-released after noise exposure, and the excitotoxicity of the excessive glutamate may be one of the injury mechanisms for the lesion of afferent nerve endings underlying IHCs caused by noise exposure.