The sensitivity of mechanoelectrical transduction response phase to acoustic overstimulation is calcium-dependent.

IF 2.9 4区 医学 Q2 PHYSIOLOGY
Pierre Hakizimana
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Abstract

The Mechanoelectrical transduction (MET) channels of the mammalian hair cells are essential for converting sound stimuli into electrical signals that enable hearing. However, the impact of acoustic overstimulation, a leading cause of hearing loss, on the MET channel function remains poorly understood. In this study, I investigated the effect of loud sound-induced temporary threshold shift (TTS) on the transduction response phase across a wide range of sound frequencies and amplitudes. The results demonstrated an increase in the transduction response phase following TTS, indicating altered transduction apparatus function. Further investigations involving the reduction of extracellular calcium, a known consequence of TTS, replicated the observed phase changes. Additionally, reduction of potassium entry confirmed the specific role of calcium in regulating the transduction response phase. These findings provide novel insights into the impact of loud sound exposure on hearing impairment at the transduction apparatus level and highlight the critical role of calcium in modulating sound transduction. Considering that over 1 billion teenagers and young adults globally are at risk of hearing loss due to unsafe music listening habits, these results could significantly enhance awareness about the damaging effects of loud sound exposure.

Abstract Image

机电转导反应阶段对声过度刺激的敏感性是钙依赖的。
哺乳动物毛细胞的机电转导(MET)通道对于将声音刺激转化为使听力成为可能的电信号至关重要。然而,作为听力损失的主要原因,声学过度刺激对MET通道功能的影响仍然知之甚少。在这项研究中,我研究了响亮的声音引起的临时阈值移位(TTS)在广泛的声音频率和振幅范围内对转导反应阶段的影响。结果显示,TTS后转导反应期增加,表明转导装置功能改变。进一步的研究涉及到细胞外钙的减少,这是TTS的一个已知后果,重复了观察到的相变。此外,钾输入的减少证实了钙在调节转导反应阶段中的特殊作用。这些发现提供了新的见解,在转导器官水平上,大声暴露对听力障碍的影响,并强调了钙在调节声音转导中的关键作用。考虑到全球有超过10亿青少年和年轻人因不安全的听音乐习惯而面临听力损失的风险,这些结果可以显著提高人们对大声接触的破坏性影响的认识。
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来源期刊
CiteScore
8.80
自引率
2.20%
发文量
121
审稿时长
4-8 weeks
期刊介绍: Pflügers Archiv European Journal of Physiology publishes those results of original research that are seen as advancing the physiological sciences, especially those providing mechanistic insights into physiological functions at the molecular and cellular level, and clearly conveying a physiological message. Submissions are encouraged that deal with the evaluation of molecular and cellular mechanisms of disease, ideally resulting in translational research. Purely descriptive papers covering applied physiology or clinical papers will be excluded. Papers on methodological topics will be considered if they contribute to the development of novel tools for further investigation of (patho)physiological mechanisms.
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