Otolaryngology Research Institute, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Department of Neonatal Pediatrics, Children's Hospital, Xiamen, China.
Neuroscience. 2019 Feb 21;400:62-71. doi: 10.1016/j.neuroscience.2018.12.048. Epub 2019 Jan 4.
Since the first report of noise-induced synaptic damage in animals without permanent threshold shifts (PTSs), the concept of noise-induced hidden hearing loss (NIHHL) has been proposed to cover the functional deficits in hearing associated with noise-induced synaptopathy. Moreover, the potential functional deficit associated with the noise-induced synaptopathy has been largely attributed to the loss of auditory nerve fibers (ANFs) with a low spontaneous spike rate (SSR). As this group of ANFs is critical for coding at suprathreshold levels and in noisy background, coding-in-noise deficit (CIND) has been considered to be main consequence of the synaptopathy. However, such deficits have not been verified after a single, brief exposure to noise without PTS. In the present study, synaptopathy was generated by such noise exposure in both mice and guinea pigs. Responses to amplitude modulation (AM) were recorded at a high sound level in combination with masking to evaluate the existence of CINDs that might be associated with loss of low-SSR ANFs. An overall reduction in response amplitude was seen in AM-evoked compound action potential (CAP). However, no such reduction was seen in the scalp-recorded envelope following response (EFR), suggesting a compensation due to increased central gain. Moreover, there was no significant difference in masking effect between the control and noise groups. The results suggest that either there is no significant CIND after the synaptopathy we created, or the AM response tested with our protocol was not sufficiently sensitive to detect such a deficit; far-field EFR is not sensitive to cochlear pathology.
自首次报道动物在未发生永久性阈移（PTS）的情况下出现噪声诱导的突触损伤以来，人们提出了噪声诱导隐匿性听力损失（NIHHL）的概念，以涵盖与噪声诱导突触病相关的听力功能缺陷。此外，与噪声诱导突触病相关的潜在功能缺陷主要归因于自发性尖峰率（SSR）较低的听神经纤维（ANF）的丧失。由于这群 ANF 对阈上水平和嘈杂背景下的编码至关重要，因此编码噪声缺陷（CIND）被认为是突触病的主要后果。然而，在没有 PTS 的单次短暂噪声暴露后，尚未验证这些缺陷是否存在。在本研究中，通过在小鼠和豚鼠中进行这种噪声暴露来产生突触病。在高声级结合掩蔽的情况下记录对幅度调制（AM）的反应，以评估可能与低 SSR ANF 丧失相关的 CIND 的存在。在 AM 诱发的复合动作电位（CAP）中观察到反应幅度的整体降低。然而，在响应后的头皮记录包络（EFR）中没有观察到这种降低，这表明由于中枢增益增加而产生了代偿。此外，对照组和噪声组之间的掩蔽效应没有显著差异。结果表明，我们所创建的突触病后要么没有明显的 CIND，要么我们的方案所测试的 AM 反应不够敏感，无法检测到这种缺陷；远场 EFR 对耳蜗病变不敏感。
