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中红外光子通过激活听觉皮层中的KCNQ2通道减轻耳鸣。

Mid-Infrared Photons Alleviate Tinnitus by Activating the KCNQ2 Channel in the Auditory Cortex.

作者信息

Liu Peng, Xue Xinmiao, Zhang Chi, Zhou Hanwen, Ding Zhiwei, Wang Li, Jiang Yuke, Zhang Zhixin, Shen Weidong, Yang Shiming, Wang Fangyuan

机构信息

Senior Department of Otolaryngology Head and Neck Surgery, the 6th Medical Center of Chinese PLA General Hospital, Chinese PLA Medical School, Beijing 100853, China.

State Key Laboratory of Hearing and Balance Science, Beijing 100853, China.

出版信息

Research (Wash D C). 2024 Sep 18;7:0479. doi: 10.34133/research.0479. eCollection 2024.

DOI:10.34133/research.0479
PMID:39296986
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11408936/
Abstract

Tinnitus is a phantom auditory sensation often accompanied by hearing loss, cognitive impairments, and psychological disturbances in various populations. Dysfunction of KCNQ2 and KCNQ3 channels-voltage-dependent potassium ion channels-in the cochlear nucleus can cause tinnitus. Despite the recognized significance of KCNQ2 and KCNQ3 channels in the auditory cortex, their precise relationship and implications in the pathogenesis of tinnitus remain areas of scientific inquiry. This study aimed to elucidate the pathological roles of KCNQ2 and KCNQ3 channels within the auditory cortex in tinnitus development and examine the therapeutic potential of mid-infrared photons for tinnitus treatment. We utilized a noise-induced tinnitus model combined with immunofluorescence, electrophysiological recording, and molecular dynamic simulation to investigate the morphological and physiological alterations after inducing tinnitus. Moreover, in vivo irradiation was administered to verify the treatment effects of infrared photons. Tinnitus was verified by deficits of the gap ratio with similar prepulse inhibition ratio and auditory brainstem response threshold. We observed an important enhancement in neuronal excitability in the auditory cortex using patch-clamp recordings, which correlated with KCNQ2 and KCNQ3 channel dysfunction. After irradiation with infrared photons, excitatory neuron firing was inhibited owing to increased KCNQ2 current resulting from structural alterations in the filter region. Meanwhile, deficits of the acoustic startle response in tinnitus animals were alleviated by infrared photons. Furthermore, infrared photons reversed the abnormal hyperexcitability of excitatory neurons in the tinnitus group. This study provided a novel method for modulating neuron excitability in the auditory cortex using KCNQ2 channels through a nonthermal effect. Infrared photons effectively mitigated tinnitus-related behaviors by suppressing abnormal neural excitability, potentially laying the groundwork for innovative therapeutic approaches for tinnitus treatment.

摘要

耳鸣是一种幻听感觉，在不同人群中常伴有听力损失、认知障碍和心理障碍。耳蜗核中KCNQ2和KCNQ3通道（电压依赖性钾离子通道）功能失调可导致耳鸣。尽管KCNQ2和KCNQ3通道在听觉皮层中的重要性已得到认可，但其在耳鸣发病机制中的精确关系和影响仍是科学研究的领域。本研究旨在阐明听觉皮层中KCNQ2和KCNQ3通道在耳鸣发生发展中的病理作用，并研究中红外光子治疗耳鸣的潜力。我们利用噪声诱导的耳鸣模型，结合免疫荧光、电生理记录和分子动力学模拟，研究耳鸣诱导后的形态学和生理学变化。此外，进行体内照射以验证红外光子的治疗效果。通过具有相似的预脉冲抑制率和听觉脑干反应阈值的间隙比缺陷来验证耳鸣。我们使用膜片钳记录观察到听觉皮层中神经元兴奋性有重要增强，这与KCNQ2和KCNQ3通道功能失调相关。在用红外光子照射后，由于滤器区域结构改变导致KCNQ2电流增加，兴奋性神经元放电受到抑制。同时，红外光子减轻了耳鸣动物的听觉惊吓反应缺陷。此外，红外光子逆转了耳鸣组兴奋性神经元的异常过度兴奋。本研究提供了一种通过非热效应利用KCNQ2通道调节听觉皮层神经元兴奋性的新方法。红外光子通过抑制异常神经兴奋性有效减轻了耳鸣相关行为，可能为耳鸣治疗的创新治疗方法奠定基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45e4/11408936/a528c25917fa/research.0479.fig.007.jpg
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