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Ribbon Synapse Plasticity in the Cochleae of Guinea Pigs after Noise-Induced Silent Damage

机译:噪声诱发的沉默损伤后豚鼠耳蜗的带状突触可塑性

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摘要

Noise exposure at low levels or low doses can damage hair cell afferent ribbon synapses without causing permanent threshold shifts. In contrast to reports in the mouse cochleae, initial damage to ribbon synapses in the cochleae of guinea pigs is largely repairable. In the present study, we further investigated the repair process in ribbon synapses in guinea pigs after similar noise exposure. In the control samples, a small portion of afferent synapses lacked synaptic ribbons, suggesting the co-existence of conventional no-ribbon and ribbon synapses. The loss and recovery of hair cell ribbons and post-synaptic densities (PSDs) occurred in parallel, but the recovery was not complete, resulting in a permanent loss of less than 10% synapses. During the repair process, ribbons were temporally separated from the PSDs. A plastic interaction between ribbons and postsynaptic terminals may be involved in the reestablishment of synaptic contact between ribbons and PSDs, as shown by location changes in both structures. Synapse repair was associated with a breakdown in temporal processing, as reflected by poorer responses in the compound action potential (CAP) of auditory nerves to time-stress signals. Thus, deterioration in temporal processing originated from the cochlea. This deterioration developed with the recovery in hearing threshold and ribbon synapse counts, suggesting that the repaired synapses had deficits in temporal processing.
机译:低水平或低剂量的噪声暴露可能会损坏毛细胞传入的带状突触而不会引起永久性阈值漂移。与小鼠耳蜗中的报道相反,豚鼠耳蜗中的带状突触的最初损伤在很大程度上可修复。在本研究中,我们进一步研究了类似噪声暴露后豚鼠丝带突触的修复过程。在对照样品中,一小部分传入突触缺乏突触带,表明常规的无丝带突触和带突触并存。毛细胞细胞带的丢失和恢复以及突触后密度(PSD)并行发生,但恢复不完全,导致永久丢失的突触少于10%。在修复过程中,色带在时间上与PSD分开。丝带和突触后末端之间的塑性相互作用可能参与丝带和PSD之间突触接触的重建,如两个结构的位置变化所示。突触修复与时间过程的破坏有关,这反映在听神经对时间压力信号的复合动作电位(CAP)响应较差的情况下。因此,时间处理的恶化源自耳蜗。这种恶化随着听力阈值和带状突触计数的恢复而发展,这表明修复的突触在时间加工方面存在缺陷。

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