Noise-Induced Hearing Loss in Gerbil: Round Window Assays of Synapse Loss.
Noise-Induced Hearing Loss in Gerbil: Round Window Assays of Synapse Loss.
复制标题
DOI：
10.3389/fncel.2021.699978
复制
发表时间：
2021
影响因子：
5.3
通讯作者：
Kujawa SG
中科院分区：
文献类型：
--
作者：
Jeffers PWC;Bourien J;Diuba A;Puel JL;Kujawa SG
先前对听力阈值恢复但噪音后内毛细胞突触永久性丧失的动物进行的研究表明，低自发率（SR）听觉神经纤维（ANF）最初很脆弱。由于这些纤维具有有助于在连续噪声背景下进行稳健声音编码的响应特性，因此它们的目标损耗将对功能产生重要影响。为了解决噪音后 ANF 相对脆弱性的问题，我们评估了沙鼠（一种按 SR 类别具有良好特征的听觉神经元分布的物种）中临时阈值偏移产生的声音过度暴露的耳蜗生理和组织学后果。噪声暴露针对具有分布式神经支配的耳蜗区域（低、中和高 SR 神经元）。它使该区域基于外毛细胞的畸变产物耳声发射和全神经复合动作电位阈值适度升高，同时伴随着阈上反应幅度的降低（在 24 小时时量化）。这些响应参数随着暴露时间的推移恢复得很好。慢性突触损失在噪声最初针对的频率区域中最大。耳蜗圆窗记录的质量电位（自发神经噪声和声音驱动的刺激周围时间反应，PSTR）反映了传统分析未检测到的损失参数。自发活动急剧减少。稳态（PSTR 平台）活动与高浓度低 SR 神经元的频率区域中的突触损失相关，而 PSTR 起始峰值和自发圆窗噪声均由高 SR 纤维活动主导，在慢性耳朵中随频率变化相对不变。总之，结果表明噪声的急性目标是混合 SR 亚型，但慢性目标主要是低 SR 神经元。 PSTR 捕获了听神经反应和损伤脆弱性的关键特性，这些特性应该在导致耳蜗突触和神经损失的听力损失病因学中产生重要的诊断信息。
Previous work in animals with recovered hearing thresholds but permanent inner hair cell synapse loss after noise have suggested initial vulnerability of low spontaneous rate (SR) auditory nerve fibers (ANF). As these fibers have properties of response that facilitate robust sound coding in continuous noise backgrounds, their targeted loss would have important implications for function. To address the issue of relative ANF vulnerabilities after noise, we assessed cochlear physiologic and histologic consequences of temporary threshold shift-producing sound over-exposure in the gerbil, a species with well-characterized distributions of auditory neurons by SR category. The noise exposure targeted a cochlear region with distributed innervation (low-, medium- and high-SR neurons). It produced moderate elevations in outer hair cell-based distortion-product otoacoustic emission and whole nerve compound action potential thresholds in this region, with accompanying reductions in suprathreshold response amplitudes, quantified at 24 h. These parameters of response recovered well with post-exposure time. Chronic synapse loss was maximum in the frequency region initially targeted by the noise. Cochlear round window recorded mass potentials (spontaneous neural noise and sound-driven peri-stimulus time responses, PSTR) reflected parameters of the loss not detected by the conventional assays. Spontaneous activity was acutely reduced. Steady-state (PSTR plateau) activity was correlated with synapse loss in frequency regions with high concentrations of low-SR neurons, whereas the PSTR onset peak and spontaneous round window noise, both dominated by high-SR fiber activity, were relatively unaltered across frequency in chronic ears. Together, results suggest that acute targets of noise were of mixed SR subtypes, but chronic targets were predominantly low-SR neurons. PSTRs captured key properties of the auditory nerve response and vulnerability to injury that should yield important diagnostic information in hearing loss etiologies producing cochlear synaptic and neural loss.
登录
查看更多内容
影响因子：
4.6
作者：
Hickman TT;Smalt C;Bobrow J;Quatieri T;Liberman MC
通讯作者：
Liberman MC
影响因子：
3
作者：
Bharadwaj HM;Verhulst S;Shaheen L;Liberman MC;Shinn-Cunningham BG
通讯作者：
Shinn-Cunningham BG
影响因子：
16.2
作者：
Beutner, D;Voets, T;Moser, T
通讯作者：
Moser, T
DOI：
10.1523/jneurosci.2845-09.2009
发表时间：
2009-11-11
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Kujawa SG;Liberman MC
通讯作者：
Liberman MC
影响因子：
2.5
作者：
Bourien, Jerome;Tang, Yong;Wang, Jing
通讯作者：
Wang, Jing