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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Nuclear factor kappaB deficiency is associated with auditory nerve degeneration and increased noise-induced hearing loss.
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Nuclear factor kappaB deficiency is associated with auditory nerve degeneration and increased noise-induced hearing loss.

机译：核因子κB缺乏与听觉神经变性和增加的噪声引起的听力损失有关。

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Degeneration of the spiral ganglion neurons (SGNs) of the auditory nerve occurs with age and in response to acoustic injury. Histopathological observations suggest that the neural degeneration often begins with an excitotoxic process affecting the afferent dendrites under the inner hair cells (IHCs), however, little is known about the sequence of cellular or molecular events mediating this excitotoxicity. Nuclear factor kappaB (NFkappaB) is a transcription factor involved in regulating inflammatory responses and apoptosis in many cell types. NFkappaB is also associated with intracellular calcium regulation, an important factor in neuronal excitotoxicity. Here, we provide evidence that NFkappaB can play a central role in the degeneration of SGNs. Mice lacking the p50 subunit of NFkappaB (p50(-/-) mice) showed an accelerated hearing loss with age that was highly associated with an exacerbated excitotoxic-like damage in afferent dendrites under IHCs and an accelerated loss of SGNs. Also, as evidenced by immunostaining intensity, calcium-buffering proteins were significantly elevated in SGNs of the p50(-/-) mice. Finally, the knock-out mice exhibited an increased sensitivity to low-level noise exposure. The accelerated hearing loss and neural degeneration with age in the p50(-/-) mice occurred in the absence of concomitant hair cell loss and decline of the endocochlear potential. These results indicate that NFkappaB activity plays an important role in protecting the primary auditory neurons from excitotoxic damage and age-related degeneration. A possible mechanism underlying this protection is that the NFkappaB activity may help to maintain calcium homeostasis in SGNs.
机译：随着年龄和响应声损伤，听觉神经的螺旋神经节神经元（SGNS）的退化发生。组织病理学观察表明，神经变性通常始于影响内毛细胞（IHC）下的传入树枝状的兴奋毒性过程，然而，关于介导这种兴奋毒性的细胞或分子事件的序列很少。核因子κB（NFKAPPAB）是参与调节许多细胞类型中炎症反应和细胞凋亡的转录因子。 NFKappab还与细胞内钙调节有关，是神经元兴奋毒性的重要因素。在这里，我们提供了证据表明，NFKappab可以在SGN的退化中发挥重要作用。缺乏NFKappab的P50亚基的小鼠（P50（ - / - ）小鼠）显示出加速的听力损失，其年龄与IHCS下传入树枝状的加剧的兴奋毒性样损伤高，并且加速丧失SGNS。此外，如通过免疫染色强度所证明的，在P50（/ - ）小鼠的SGN中显着升高了钙缓冲蛋白。最后，敲除小鼠对低水平噪声暴露的敏感性增加了。在没有伴随的毛细胞损失和内孔潜力下降的情况下发生了P50（ - / - ）小鼠的加速听力损失和患年龄的神经变性。这些结果表明，NFKappab活性在保护兴奋毒性损伤和年龄相关变性中的主要听觉神经元中起着重要作用。这种保护的可能机制是NFKappab活动可能有助于在SGNS中维持钙稳态。

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