Efferent neurons control hearing sensitivity and protect hearing from noise through the regulation of gap junctions between cochlear supporting cells.
Efferent neurons control hearing sensitivity and protect hearing from noise through the regulation of gap junctions between cochlear supporting cells.
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DOI：
10.1152/jn.00468.2021
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发表时间：
2021-12
影响因子：
2.5
通讯作者：
Hong-Bo Zhao;Li-Man Liu;N. Yu;Yan Zhu;Ling Mei;Jin Chen;Chun Liang
中科院分区：
文献类型：
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作者：
Hong-Bo Zhao;Li-Man Liu;N. Yu;Yan Zhu;Ling Mei;Jin Chen;Chun Liang
耳蜗下行传出神经系统对毛细胞的负反馈调节听觉灵敏度，保护听力免受噪声的影响，这对听力至关重要。在这里，我们报告的内侧橄榄耳蜗（MOC）传出神经，它的项目外毛细胞（OHC），也可以支配周围的支持细胞（SC）的OHC调节听力。MOC神经纤维是胆碱能的，乙酰胆碱（ACh）是主要的神经递质。MOC神经末梢，突触前囊泡乙酰胆碱转运体（VAChT），和突触后ACh受体可见SC和SC区。ACh在SC中的应用可以引起典型的内向电流，其减少SC之间的间隙连接（GJ），从而降低OHC电活动性，OHC电活动性是一种主动耳蜗放大，可以增加听觉灵敏度。这种间接的GJ介导的抑制增强了ACh对OHC电活动的直接抑制，但具有持久的影响。体内实验进一步表明，缺乏这种GJ介导的传出通路下降主动耳蜗放大的调节，并损害对噪声的保护。特别是，畸变产生耳声发射（DPOAE）表现出延迟减少噪声暴露后。我们的研究结果揭示了一个新的途径为MOC传出系统通过神经支配SC控制主动耳蜗放大和听觉灵敏度。这些数据还表明，GJ介导的传出通路可能在长期传出抑制中发挥关键作用，并为保护听力免受噪声损伤所必需。
It is critical for hearing that the descending cochlear efferent system provide a negative feedback to hair cells to regulate hearing sensitivity and provide the protection of hearing from noise. Here, we report that the medial olivocochlear (MOC) efferent nerves, which project to outer hair cells (OHCs), also could innervate OHC surrounding supporting cells (SCs) to regulate hearing sensitivity. MOC nerve fibers are cholinergic and acetylcholine (ACh) is a primary neurotransmitter. MOC nerve endings, presynaptic vesicular acetylcholine transporters (VAChT), and postsynaptic ACh receptors were visible in SCs and the SC area. Application of ACh in the SC could evoke a typical inward current, which reduced gap junctions (GJs) between SCs and consequently declined OHC electromotility, which is an active cochlear amplification and can increase hearing sensitivity. This indirect, GJ-mediated inhibition enhanced the direct inhibition of ACh on OHC electromotility but had long-lasting influence. In vivo experiments further demonstrated that deficiency of this GJ-mediated efferent pathway declined the regulation of active cochlear amplification and compromised the protection against noise. In particular, distortion production otoacoustic emission (DPOAE) showed a delayed reduction after noise exposure. Our findings reveal a new pathway for the MOC efferent system via innervating SCs to control active cochlear amplification and hearing sensitivity. These data also suggest that this GJ-mediated efferent pathway may play a critical role in the long-term efferent inhibition and is required for protecting hearing from noise trauma.