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首页> 外文期刊>HNO >Water regulation in the cochlea: Do molecular water channels facilitate potassium-dependent sound transduction? [Wasserregulation in der Cochlea: Unterstützen molekulare Wasserkan?le die kaliumabh?ngige Schalltransduktion?]
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Water regulation in the cochlea: Do molecular water channels facilitate potassium-dependent sound transduction? [Wasserregulation in der Cochlea: Unterstützen molekulare Wasserkan?le die kaliumabh?ngige Schalltransduktion?]

机译:耳蜗中的水调节:分子水通道是否促进钾依赖性声音传导? [耳蜗中的水调节:分子水通道是否支持钾依赖性声音传导?]

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Background: Sound transduction in the cochlea critically depends on the circulation of potassium ions (K+) along so-called "K+ recycling routes" between the endolymph and perilymph. These K+ currents generate high ionic and osmotic gradients, which potentially impair the excitability of sensory hair cells and threaten cell survival in the entire cochlear duct. Molecular water channels-aquaporins (AQP)-are expressed in all cochlear supporting cells along the K+ recycling routes; however, their significance for osmotic equilibration in cochlear duct cells is unknown. Methods: The diffusive and osmotic water permeabilies of Reissner's membrane, the organ of Corti and the entire cochlear duct epithelium were determined. Expression of the potassium channel Kir4.1 and the water channel AQP4 in the cochlear duct was investigated by immunohistochemistry. Results: The calculated water permeability values indicate the extent of AQP-facilitated water flux across the cochlear duct epithelium. Immunohistochemically, Kir4.1 and AQP4 were found to colocalize in distinct membrane domains of supporting cells along the K+-recycling routes. Conclusion: These observations suggest the presence of a rapid AQP-mediated water exchange between the endolymph, the cells of the cochlear duct and the perilymph. The subcellular colocalization of Kir4.1 and AQP4 in epithelial supporting cells indicates functional coupling of potassium and water flow in the cochlea. Finally, this offers an explanation for the hearing impairment observed in individuals with mutations in the AQP4 gene.
机译:背景:耳蜗中的声音传导主要取决于内淋巴和外淋巴之间钾离子(K +)沿所谓的“ K +循环途径”的循环。这些K +电流会产生高离子和渗透梯度,这可能会损害感觉毛细胞的兴奋性并威胁整个耳蜗管中的细胞存活。分子水通道-水通道蛋白(AQP)-在沿K +再循环途径的所有耳蜗支持细胞中表达;但是,它们对于耳蜗管细胞中渗透平衡的意义尚不清楚。方法:测定Reissner膜,Corti器官和整个耳蜗上皮的扩散和渗透水透过率。通过免疫组织化学研究了钾通道Kir4.1和水通道AQP4在耳蜗中的表达。结果:计算出的水渗透率值表明AQP促进了整个耳蜗上皮水通量。免疫组织化学研究发现,Kir4.1和AQP4沿K +循环途径共定位在支持细胞的不同膜结构域中。结论:这些观察结果表明内淋巴,耳蜗管细胞和外淋巴之间存在快速的AQP介导的水交换。 Kir4.1和AQP4在上皮支持细胞中的亚细胞共定位表明耳蜗中钾和水的功能性耦合。最后,这为在AQP4基因突变的个体中观察到的听力障碍提供了解释。

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