Cody A R, Russell I J
Nature. 1985;315(6021):662-5. doi: 10.1038/315662a0.
Hair cells in the mammalian cochlea transduce mechanical stimuli into electrical signals leading to excitation of auditory nerve fibres. Because of their important role in hearing, these cells are a possible site for the loss of cochlear sensitivity that follows acoustic overstimulation. We have recorded from inner and outer hair cells (IHC, OHC) in the guinea pig cochlea during and after exposure to intense tones. Our results show functional changes in the hair cells that may explain the origin of noise-induced hearing loss. Both populations of hair cells show a reduction in amplitude and an increase in the symmetry of their acoustically evoked receptor potentials. In addition, the OHCs also suffer a sustained depolarization of the membrane potential. Significantly, the membrane and receptor potentials of the OHCs recover in parallel with cochlear sensitivity as measured by the IHC receptor potential amplitude and the auditory nerve threshold. Current theories of acoustic transduction suggest that the mechanical input to IHCs may be regulated by the OHCs. Consequently, the modified function of OHCs after acoustic overstimulation may determine the extent of the hearing loss following loud sound.
哺乳动物耳蜗中的毛细胞将机械刺激转化为电信号，从而激发听神经纤维。由于它们在听力中起着重要作用，这些细胞可能是声学过度刺激后耳蜗敏感性丧失的一个部位。我们在豚鼠耳蜗暴露于高强度音调期间及之后，对内毛细胞和外毛细胞（IHC、OHC）进行了记录。我们的结果显示了毛细胞的功能变化，这可能解释了噪声性听力损失的起源。两类毛细胞的声诱发感受器电位幅度均降低，对称性增加。此外，外毛细胞的膜电位还出现持续去极化。值得注意的是，外毛细胞的膜电位和感受器电位与通过内毛细胞感受器电位幅度和听神经阈值测量的耳蜗敏感性同步恢复。当前的声学转导理论表明，内毛细胞的机械输入可能受外毛细胞调节。因此，声学过度刺激后外毛细胞功能的改变可能决定了大声后听力损失的程度。
