A mechanism for sensing noise damage in the inner ear
A mechanism for sensing noise damage in the inner ear
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DOI：
10.1016/j.cub.2004.03.002
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发表时间：
2004-03-23
期刊：
影响因子：
9.2
通讯作者：
Mammano, F
中科院分区：
文献类型：
--
作者：
Gale, JE;Piazza, V;Mammano, F
我们的听觉需要功能性的感觉毛细胞。在整个生命过程中，这些毛细胞受到各种创伤，最常见的是响亮的声音。声损伤的主要影响表现为毛细胞静纤毛的精细机械感觉装置的损伤[1]。这可能最终导致毛细胞死亡[2]和不可逆的耳聋[3]。关于有害声音刺激影响听觉感觉上皮细胞的单个细胞成分的方式知之甚少。然而，在不同类型的细胞培养物中的研究表明，损伤和机械刺激可以激活细胞内游离钙浓度（[Ca（2+）]（i））的变化，并引发细胞间Ca（2+）波[4]。因此，一个有吸引力的假设是，[Ca（2+）]（i）的变化，作为波通过Corti器官中的支持细胞传播，可能构成了毛细胞损伤发生信号的基本机制。我们在此描述的机制表现出对细胞外ATP的纳摩尔敏感性，涉及由于来自毛细胞的ATP引起的细胞间钙波的再生传播，并依赖于支持细胞中功能性IP（3）敏感的细胞内储存。
Our sense of hearing requires functional sensory hair cells. Throughout life those hair cells are subjected to various traumas, the most common being loud sound. The primary effect of acoustic trauma is manifested as damage to the delicate mechanosensory apparatus of the hair cell stereocilia [1]. This may eventually lead to hair cell death [2] and irreversible deafness [3]. Little is known about the way in which noxious sound stimuli affect individual cellular components of the auditory sensory epithelium. However, studies in different types of cell cultures have shown that damage and mechanical stimulation can activate changes in intracellular free calcium concentration ([Ca(2+)](i)) and elicit intercellular Ca(2+) waves [4]. Thus an attractive hypothesis is that changes in [Ca(2+)](i), propagating as a wave through support cells in the organ of Corti, may constitute a fundamental mechanism to signal the occurrence of hair cell damage. The mechanism we describe here exhibits nanomolar sensitivity to extracellular ATP, involves regenerative propagation of intercellular calcium waves due to ATP originating from hair cells, and depends on functional IP(3)-sensitive intracellular stores in support cells.