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同侧宽带掩蔽下听觉脑干反应减弱作为噪声性耳蜗突触病的标志物。

Decreased Reemerging Auditory Brainstem Responses Under Ipsilateral Broadband Masking as a Marker of Noise-Induced Cochlear Synaptopathy.

机构信息

Laboratory of Neurosensory Biophysics, University Clermont Auvergne, UMR INSERM 1107, Clermont-Ferrand, France.

Centre Jean Perrin, Clermont-Ferrand, France.

出版信息

Ear Hear. 2021 July/Aug;42(4):1062-1071. doi: 10.1097/AUD.0000000000001009.

Abstract

OBJECTIVES

In mammals, a 2-hr exposure to an octave-band noise (OBN) at 100 to 108 dB SPL induces loss of synaptic ribbons between inner hair cells and auditory nerve fibers with high thresholds of response (hiT neurons), that encode high-intensity sounds. Here, we tackle the challenge of diagnosing this synaptopathy by a noninvasive functional audiological test, ultimately in humans, despite the expected absence of auditory-threshold elevation and of clear electrophysiological abnormality, hiT neuron contributions being hidden by those of more sensitive and robust neurons.

DESIGN

The noise-induced synaptopathy was replicated in mice (at 94, 97, and 100 dB SPL; n = 7, 7, and 8, respectively, against 8 unexposed controls), without long-lasting auditory-threshold elevation despite a twofold decrease in ribbon-synapse number for the 100-dB OBN exposure. Auditory brainstem responses (ABRs) were collected using a simultaneous broadband noise masker just able to erase the ABR response to a 60-dB tone burst. Tone burst intensity was then increased up to 100 dB SPL for eliciting reemerging ABRs (R-ABRs), dependent on hiT neurons as more sensitive neurons are masked.

RESULTS

In most ears exposed to 97-dB-SPL and all ears exposed to 100-dB-SPL OBN, contrary to controls, R-ABRs from the overexposed region have vanished, whereas standard ABR distributions widely overlap.

CONCLUSIONS

R-ABRs afford an individual noninvasive marker of normal-auditory-threshold cochlear synaptopathy. A simple modification of standard ABRs would allow hidden auditory synaptopathy to be searched in a patient.

ABBREVIATIONS

ABR: auditory brainstem response; dB SPL: decibel sound pressure level; DPOAE: distortion-product otoacoustic emission; hiT neuron: high-threshold neuron; IHC: inner hair cell; loT neuron: low-threshold neuron; OBN: octave-band noise; OHC: outer hair cell; PBS: phosphate buffer saline; R-ABR: reemerging ABR.

摘要

目的

在哺乳动物中,100 至 108 分贝声压级的倍频程噪声(OBN)暴露 2 小时会导致内毛细胞和听觉神经纤维之间的突触带丢失,这些纤维对高阈值的反应(高阈值神经元,hiT 神经元)进行编码高强度声音。在这里,我们通过非侵入性功能听力学测试来应对诊断这种突触病的挑战,最终在人类中进行,尽管预计不会出现听觉阈值升高和明显的电生理异常,hiT 神经元的贡献被更敏感和更稳健的神经元所掩盖。

设计

在小鼠中复制了噪声诱导的突触病(在 94、97 和 100 分贝声压级下;分别为 7、7 和 8 只,而 8 只未暴露的对照组),尽管 100 分贝 OBN 暴露导致突触数量减少了两倍,但没有出现长期的听觉阈值升高。使用同时的宽带噪声掩蔽器收集听觉脑干反应(ABR),该掩蔽器刚好能够擦除对 60 分贝短音爆发的 ABR 反应。然后增加短音爆发强度,直至 100 分贝声压级,以引出重新出现的 ABR(R-ABR),这取决于 hiT 神经元,因为更敏感的神经元被掩蔽。

结果

在大多数暴露于 97 分贝声压级的耳朵和所有暴露于 100 分贝声压级 OBN 的耳朵中,与对照组相反,过度暴露区域的 R-ABR 已经消失,而标准 ABR 分布则广泛重叠。

结论

R-ABR 为正常听觉阈值耳蜗突触病提供了个体的非侵入性标志物。对标准 ABRs 的简单修改将允许在患者中搜索隐藏的听觉突触病。

缩写词

ABR:听觉脑干反应;dB SPL:分贝声压级;DPOAE:失真产物耳声发射;hiT 神经元:高阈值神经元;IHC:内毛细胞;loT 神经元:低阈值神经元;OBN:倍频程噪声;OHC:外毛细胞;PBS:磷酸盐缓冲盐水;R-ABR:重新出现的 ABR。

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