Inner Hair Cell Loss Disrupts Hearing and Cochlear Function Leading to Sensory Deprivation and Enhanced Central Auditory Gain.
Inner Hair Cell Loss Disrupts Hearing and Cochlear Function Leading to Sensory Deprivation and Enhanced Central Auditory Gain.
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DOI：
10.3389/fnins.2016.00621
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发表时间：
2016
影响因子：
4.3
通讯作者：
Auerbach BD
中科院分区：
文献类型：
--
作者：
Salvi R;Sun W;Ding D;Chen GD;Lobarinas E;Wang J;Radziwon K;Auerbach BD
外毛细胞 (OHC) 的数量是内毛细胞 (IHC) 的三倍，但 IHC 几乎将所有声音信息传输到大脑，因为它们与 90-95% 的 I 型听觉神经纤维形成突触。在这里，我们回顾了一系列全面的实验，旨在通过使用耳毒性抗癌剂卡铂选择性破坏龙猫中的这些细胞来确定 IHC/I 型系统的丧失如何影响听力。消除 IHC/I 型神经元对畸变产物耳声发射或 OHC 产生的耳蜗颤音电位没有影响；然而，它大大降低了 IHC 产生的求和电位和 I 型神经元产生的复合动作电位 (CAP)。值得注意的是，尽管耳蜗的神经支配区域 IHC 损失约 80%，但剩余听觉神经纤维的反应仍保持敏锐的调谐和低阈值。此外，具有大 IHC 损伤的龙猫在安静时具有令人惊讶的正常阈值，直到 IHC 损失超过 80%，这表明只需要少量 IHC 即可检测安静时的声音。然而，宽带噪声的行为阈值显着升高，并且窄带噪声掩蔽模式表现出更大的远程掩蔽。这些结果表明，听觉系统能够在安静但在困难的聆听条件下补偿 IHC/I 型神经元的大量损失。听觉大脑如何应对耳蜗输入的急剧丧失？下丘的记录发现，尽管 IHC 损伤后 CAP 振幅大幅下降，但声音诱发活动的下降幅度相对较小。矛盾的是，声音诱发的反应通常比听觉皮层的正常反应大，表明中央增益增加。听觉皮层的这种增益增强与 GABA 介导的抑制作用减少有关。这些结果表明，当耳蜗的神经输出减少时，中枢听觉系统会通过调高其增益来进行补偿，使微弱的信号再次变得舒适而响亮。虽然这种增益增强能够在安静条件下恢复正常听力，但它可能无法充分补偿更复杂的声音环境中的外围功能障碍。此外，过度的增益增加可能会将募集转化为一种称为听觉过敏的衰弱状况。
There are three times as many outer hair cells (OHC) as inner hair cells (IHC), yet IHC transmit virtually all acoustic information to the brain as they synapse with 90–95% of type I auditory nerve fibers. Here we review a comprehensive series of experiments aimed at determining how loss of the IHC/type I system affects hearing by selectively destroying these cells in chinchillas using the ototoxic anti-cancer agent carboplatin. Eliminating IHC/type I neurons has no effect on distortion product otoacoustic emission or the cochlear microphonic potential generated by OHC; however, it greatly reduces the summating potential produced by IHC and the compound action potential (CAP) generated by type I neurons. Remarkably, responses from remaining auditory nerve fibers maintain sharp tuning and low thresholds despite innervating regions of the cochlea with ~80% IHC loss. Moreover, chinchillas with large IHC lesions have surprisingly normal thresholds in quiet until IHC losses exceeded 80%, suggesting that only a few IHC are needed to detect sounds in quiet. However, behavioral thresholds in broadband noise are elevated significantly and tone-in-narrow band noise masking patterns exhibit greater remote masking. These results suggest the auditory system is able to compensate for considerable loss of IHC/type I neurons in quiet but not in difficult listening conditions. How does the auditory brain deal with the drastic loss of cochlear input? Recordings from the inferior colliculus found a relatively small decline in sound-evoked activity despite a large decrease in CAP amplitude after IHC lesion. Paradoxically, sound-evoked responses are generally larger than normal in the auditory cortex, indicative of increased central gain. This gain enhancement in the auditory cortex is associated with decreased GABA-mediated inhibition. These results suggest that when the neural output of the cochlea is reduced, the central auditory system compensates by turning up its gain so that weak signals once again become comfortably loud. While this gain enhancement is able to restore normal hearing under quiet conditions, it may not adequately compensate for peripheral dysfunction in more complex sound environments. In addition, excessive gain increases may convert recruitment into the debilitating condition known as hyperacusis.