Department of Otology and Laryngology, Harvard Medical School, Boston, MA, USA.
J Assoc Res Otolaryngol. 2011 Oct;12(5):605-16. doi: 10.1007/s10162-011-0277-0. Epub 2011 Jun 18.
Recent work in mouse showed that acoustic overexposure can produce a rapid and irreversible loss of cochlear nerve peripheral terminals on inner hair cells (IHCs) and a slow degeneration of spiral ganglion cells, despite full recovery of cochlear thresholds and no loss of inner or outer hair cells (Kujawa and Liberman, J Neurosci 29:14077-14085, 2009). This contrasts with earlier ultrastructural work in guinea pig suggesting that acute noise-induced neural degeneration is followed by full regeneration of cochlear nerve terminals in the IHC area (Puel et al., Neuroreport 9:2109-2114, 1998; Pujol and Puel, Ann N Y Acad Sci 884:249-254, 1999). Here, we show that the same patterns of primary neural degeneration reported for mouse are also seen in the noise-exposed guinea pig, when IHC synapses and cochlear nerve terminals are counted 1 week post-exposure in confocal images from immunostained whole mounts and that the same slow degeneration of spiral ganglion cells occurs despite no loss of IHCs and apparent recovery of cochlear thresholds. The data cast doubt on prior claims that there is significant neural regeneration and synaptogenesis in the adult cochlea and suggest that denervation of the inner hair cell is an important sequela of "reversible" noise-induced hearing loss, which likely applies to the human ear as well.
最近在小鼠中的研究工作表明，尽管耳蜗阈值完全恢复且内毛细胞和外毛细胞没有损失，但过度的声暴露会导致内毛细胞（IHC）上的耳蜗神经末梢快速且不可逆转地丧失，并导致螺旋神经节细胞缓慢退化（Kujawa 和 Liberman，J Neurosci 29:14077-14085，2009）。这与早期豚鼠的超微结构研究工作形成对比，后者表明急性噪声诱导的神经退化之后，内毛细胞区域的耳蜗神经末梢会完全再生（Puel 等人，Neuroreport 9:2109-2114，1998；Pujol 和 Puel，Ann N Y Acad Sci 884:249-254，1999）。在这里，我们表明，在暴露于噪声的豚鼠中也可以看到与小鼠中报道的相同的初级神经退化模式，当在免疫染色的全距标本的共聚焦图像中计算暴露后 1 周的 IHC 突触和耳蜗神经末梢时，以及当发生相同的螺旋神经节细胞缓慢退化时，尽管 IHC 没有损失且耳蜗阈值明显恢复。这些数据对先前有关成年耳蜗中存在显著神经再生和突触发生的说法提出了质疑，并表明内毛细胞的去神经支配是“可逆”噪声性听力损失的重要后果，这可能也适用于人耳。
