Permanent threshold shift caused by acute cochlear mitochondrial dysfunction is primarily mediated by degeneration of the lateral wall of the cochlea
Permanent threshold shift caused by acute cochlear mitochondrial dysfunction is primarily mediated by degeneration of the lateral wall of the cochlea
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DOI：
10.1159/000084843
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发表时间：
2005-01-01
影响因子：
1.6
通讯作者：
Matsunaga, T
中科院分区：
文献类型：
--
作者：
Okamoto, Y;Hoya, N;Matsunaga, T
耳蜗线粒体功能障碍被认为是感音神经性听力损失的重要原因。最近，我们建立了一种新的急性听力损伤的大鼠模型暴露于线粒体毒素3-硝基丙酸（3-NP），以分析耳蜗线粒体功能障碍的机制。在该模型中观察到永久性和暂时性阈值偏移，这取决于用于诱导听力损伤的3-NP的量。在这项研究中，我们证明耳蜗形态学的变化，在永久性阈值漂移模型。在3-NP给药后3 h，在螺旋突起中的2型纤维细胞、螺旋韧带中的4型纤维细胞、血管纹中的边缘细胞和中间细胞中检测到明显的变性;这些变化进行性至少14天。在螺旋韧带中的1型和3型纤维细胞中检测到不太明显的变性。这些结果表明，急性耳蜗线粒体功能障碍引起的永久性阈移主要是由耳蜗外侧壁细胞变性介导的，并建议通过保护和再生耳蜗外侧壁来实现急性能量衰竭引起的耳蜗听力损失的治疗。版权所有（C）2005 S. Karger AG，巴塞尔。
Mitochondrial dysfunction in the cochlea is thought to be an important cause of sensorineural hearing loss. Recently, we have established a novel rat model with acute hearing impairment caused by exposure to the mitochondrial toxin 3-nitropropionic acid (3-NP) to analyze the mechanism of cochlear mitochondrial dysfunction. Both permanent and temporary threshold shifts were observed in this model depending on the amount of 3-NP used to induce hearing impairment. In this study, we demonstrate cochlear morphological changes in the permanent threshold shift model. Marked degeneration was detected in type 2 fibrocytes in the spiral prominence, type 4 fibrocytes in the spiral ligament, marginal cells and intermediate cells in the stria vascularis 3 h after 3-NP administration; these changes were progressive for at least 14 days. Less prominent degeneration was detected in type 1 and type 3 fibrocytes in the spiral ligament. These results indicate that permanent threshold shift caused by acute cochlear mitochondrial dysfunction is primarily mediated by cellular degeneration in the lateral wall of the cochlea, and suggest that therapy of cochlear hearing loss due to acute energy failure may be achieved through protection and regeneration of the cochlear lateral wall. Copyright (C) 2005 S. Karger AG, Basel.