Recovery of endocochlear potential after severe damage to lateral wall fibrocytes following acute cochlear energy failure
Recovery of endocochlear potential after severe damage to lateral wall fibrocytes following acute cochlear energy failure
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DOI：
10.1097/wnr.0000000000000673
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发表时间：
2016-10-19
期刊：
影响因子：
1.7
通讯作者：
Fujii, Masato
中科院分区：
文献类型：
--
作者：
Kitao, Kyoko;Mizutari, Kunio;Fujii, Masato
耳蜗内电位降低是感音神经性耳聋的主要原因之一。在这项研究中，我们使用了一个急性耳蜗能量衰竭的小鼠模型来研究EP的变化，其中包括内耳局部注射3-硝基丙酸导致的严重耳蜗侧壁损伤。我们还分析了EP变化与耳蜗侧壁组织学改变的相关性。检测相应区域耳蜗侧壁成纤维细胞严重损伤后诱发电位和低频听力功能的恢复情况。耳蜗侧壁重塑与EP恢复有关，包括离子转运体或缝隙连接蛋白(即Na+/K+/ATPase-1和连接蛋白26)的重新表达。这些结果表明，严重耳聋后的晚期听力恢复是一种机制，这在临床环境中经常被观察到。
Reduction of endocochlear potential (EP) is one of the main causes of sensorineural hearing loss. In this study, we investigated changes in the EP using a mouse model of acute cochlear energy failure, which comprised severe cochlear lateral wall damage induced by the local administration of 3-nitropropionic acid to the inner ear. We also analyzed the correlation between EP changes and histological findings in the cochlear lateral wall. We detected the recovery of the EP and hearing function at lower frequencies after severe damage of the cochlear lateral wall fibrocytes at the corresponding region. Remodeling of the cochlear lateral wall was associated with EP recovery, including the re-expression of ion transporters or gap junctions (i.e. Na+/K+/ATPase-1 and connexin 26). These results indicate a mechanism for late-phase hearing recovery after severe deafness, which is frequently observed in clinical settings.