Non-Monotonic Relation between Noise Exposure Severity and Neuronal Hyperactivity in the Auditory Midbrain
Non-Monotonic Relation between Noise Exposure Severity and Neuronal Hyperactivity in the Auditory Midbrain
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DOI：
10.3389/fneur.2016.00133
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发表时间：
2016-08-25
影响因子：
3.4
通讯作者：
Schaette, Roland
中科院分区：
文献类型：
--
作者：
Hesse, Lara Li;Bakay, Warren;Schaette, Roland
耳鸣的发生可以联系到听力损失在大多数情况下，但仍然有很大程度上无法解释的异质性之间的关系听力损失和耳鸣。部分问题可能是听力损失通常以听力阈值增加来量化，这只能提供有关潜在耳蜗损伤的有限信息。此外，不引起听力阈值损失的噪声暴露仍然会导致“隐性听力损失”（HHL），即，通过内毛细胞中突触带的损失，听觉神经纤维（ANF）的功能性传入阻滞。虽然已知增加的听力阈值可以触发中枢听觉系统中自发神经活动的增加，即，HHL是耳鸣的一种假定的神经相关物，其中枢效应尚未被研究。在这里，我们将小鼠暴露于100和105 dB SPL的倍频程噪声中，分别产生HHL和永久性听力阈值增加。通过听性脑干反应和耳蜗免疫组织化学测定证实ANF的传入阻滞。听觉中脑（下丘）的急性细胞外记录显示两组中自发神经元活动（耳鸣的假定神经相关性）增加。令人惊讶的是，自发活动的增加在患有HHL的小鼠中最为明显，这表明听力损失和神经元过度活跃之间的关系可能比目前所理解的更为复杂。我们的计算模型表明，这些差异，神经元过度活跃，可能会产生不同程度的去传入的低阈值ANF在两个曝光组。我们的研究结果表明，HHL是足以引起中枢听觉处理的变化，他们也表明耳蜗损伤和神经元过度活跃之间的非单调关系，提示耳鸣可能会发生没有明显的听力损失，相反，为什么听力损失并不总是导致耳鸣的解释。
The occurrence of tinnitus can be linked to hearing loss in the majority of cases, but there is nevertheless a large degree of unexplained heterogeneity in the relation between hearing loss and tinnitus. Part of the problem might be that hearing loss is usually quantified in terms of increased hearing thresholds, which only provides limited information about the underlying cochlear damage. Moreover, noise exposure that does not cause hearing threshold loss can still lead to "hidden hearing loss" (HHL), i.e., functional deafferentation of auditory nerve fibers (ANFs) through loss of synaptic ribbons in inner hair cells. While it is known that increased hearing thresholds can trigger increases in spontaneous neural activity in the central auditory system, i.e., a putative neural correlate of tinnitus, the central effects of HHL have not yet been investigated. Here, we exposed mice to octave-band noise at 100 and 105 dB SPL to generate HHL and permanent increases of hearing thresholds, respectively. Deafferentation of ANFs was confirmed through measurement of auditory brainstem responses and cochlear immunohistochemistry. Acute extracellular recordings from the auditory midbrain (inferior colliculus) demonstrated increases in spontaneous neuronal activity (a putative neural correlate of tinnitus) in both groups. Surprisingly, the increase in spontaneous activity was most pronounced in the mice with HHL, suggesting that the relation between hearing loss and neuronal hyperactivity might be more complex than currently understood. Our computational model indicated that these differences in neuronal hyperactivity could arise from different degrees of deafferentation of low-threshold ANFs in the two exposure groups. Our results demonstrate that HHL is sufficient to induce changes in central auditory processing, and they also indicate a non-monotonic relationship between cochlear damage and neuronal hyperactivity, suggesting an explanation for why tinnitus might occur without obvious hearing loss and conversely why hearing loss does not always lead to tinnitus.