ArticleResearch (Washington, D.C.)2024
Mid-Infrared Photons Alleviate Tinnitus by Activating the KCNQ2 Channel in the Auditory Cortex.
Article in Research (Washington, D.C.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Potential therapeutic role of calcitonin gene-related peptide medications for tinnitus.Journal of the Chinese Medical Association : JCMA · 2026Review
- Mid-infrared photons relieve tinnitus-like behavior of mice by regulating HCN2 ion channels in the medial geniculate body.Annals of medicine · 2025Article
- Dual-Omics Mapping of Tinnitus Phenotype Transition in Noise-Exposed Auditory Cortex.Cellular and molecular neurobiology · 2025Article
- Terahertz Science and Technology in Astronomy, Telecommunications, and Biophysics.Research (Washington, D.C.) · 2025Review
- Advances in Terahertz Biophysics and Chemistry.Research (Washington, D.C.) · 2025Review
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Authors and funding
11 authors.
Funding
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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.
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Registered trials
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