Department of Neuroscience, Psychology and Behavior, University of Leicester, Leicester, LE1 7RH, United Kingdom,
Department of Neuroscience, Psychology and Behavior, University of Leicester, Leicester, LE1 7RH, United Kingdom.
J Neurosci. 2020 Apr 8;40(15):3130-3140. doi: 10.1523/JNEUROSCI.2279-19.2019. Epub 2020 Mar 6.
Acoustic overexposure, such as listening to loud music too often, results in noise-induced hearing loss. The pathologies of this prevalent sensory disorder begin within the ear at synapses of the primary auditory receptors, their postsynaptic partners and their supporting cells. The extent of noise-induced damage, however, is determined by overstimulation of primary auditory receptors, upstream of where the pathologies manifest. A systematic characterization of the electrophysiological function of the upstream primary auditory receptors is warranted to understand how noise exposure impacts on downstream targets, where the pathologies of hearing loss begin. Here, we used the experimentally-accessible locust ear (male, to characterize a decrease in the auditory receptor's ability to respond to sound after noise exposure. Surprisingly, after noise exposure, the electrophysiological properties of the auditory receptors remain unchanged, despite a decrease in the ability to transduce sound. This auditory deficit stems from changes in a specialized receptor lymph that bathes the auditory receptors, revealing striking parallels with the mammalian auditory system. Noise exposure is the largest preventable cause of hearing loss. It is the auditory receptors that bear the initial brunt of excessive acoustic stimulation, because they must convert excessive sound-induced movements into electrical signals, but remain functional afterward. Here we use the accessible ear of an invertebrate to, for the first time in any animal, characterize changes in auditory receptors after noise overexposure. We find that their decreased ability to transduce sound into electrical signals is, most probably, due to changes in supporting (scolopale) cells that maintain the ionic composition of the ear. An emerging doctrine in hearing research is that vertebrate primary auditory receptors are surprisingly robust, something that we show rings true for invertebrate ears too.
声过度暴露，如经常听大音量的音乐，会导致噪声性听力损失。这种普遍的感觉障碍的病理学始于内耳的初级听觉感受器的突触，它们的突触后伙伴及其支持细胞。然而，噪声诱导损伤的程度取决于初级听觉感受器的过度刺激，而这种病理学表现之前。系统地表征上游初级听觉感受器的电生理功能对于理解噪声暴露如何影响下游靶标，即听力损失的病理学开始的地方，是有必要的。在这里，我们使用实验上可获得的蝗虫耳（雄性）来表征噪声暴露后听觉感受器对声音的响应能力下降。令人惊讶的是，噪声暴露后，听觉感受器的电生理特性仍然不变，尽管对声音的转导能力下降。这种听觉缺陷源于专门的受体淋巴液的变化，这种淋巴液包裹着听觉感受器，与哺乳动物听觉系统惊人地相似。噪声暴露是可预防的最大听力损失原因。正是听觉感受器承受了过度声刺激的最初冲击，因为它们必须将过度的声音引起的运动转化为电信号，但之后仍然保持功能。在这里，我们使用无脊椎动物的可及耳朵，首次在任何动物中，在噪声过度暴露后对听觉感受器的变化进行了表征。我们发现，它们将声音转化为电信号的能力下降，很可能是由于维持耳朵离子组成的支持（栉状）细胞发生了变化。听觉研究中的一个新兴学说认为，脊椎动物的初级听觉感受器出人意料地强壮，我们发现这对无脊椎动物的耳朵也是如此。
