In the cochlea, K(+) is essential for mechano-electrical transduction. Here, we explore cochlear structure and function in mice lacking K(+) channels of the two-pore domain family. A profound deafness associated with a decrease in endocochlear potential is found in adult Kcnk5(-/-) mice. Hearing occurs around postnatal day 19 (P19), and completely disappears 2 days later. At P19, Kcnk5(-/-) mice have a normal endolymphatic [K(+)] but a partly lowered endocochlear potential. Using Lac-Z as a gene reporter, KCNK5 is mainly found in outer sulcus Claudius', Boettcher's and root cells. Low levels of expression are also seen in the spiral ganglion, Reissner's membrane and stria vascularis. Essential channels (KCNJ10 and KCNQ1) contributing to K(+) secretion in stria vascularis have normal expression in Kcnk5(-/-) mice. Thus, KCNK5 channels are indispensable for the maintenance of hearing. Among several plausible mechanisms, we emphasize their role in K(+) recycling along the outer sulcus lateral route.

中文翻译：

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大部分在耳蜗外沟细胞中表达的KCNK5通道对于听力是必不可少的。

在耳蜗中，K（+）对于机电转换至关重要。在这里，我们探索缺少两孔域家族的K（+）通道的小鼠的耳蜗结构和功能。在成年Kcnk5（-/-）小鼠中发现了与耳蜗电位降低相关的严重耳聋。听力发生在出生后第19天（P19）左右，并在2天后完全消失。在P19处，Kcnk5（-/-）小鼠具有正常的内淋巴管[K（+）]，但部分降低了耳蜗的内耳电位。使用Lac-Z作为基因报告基因，KCNK5主要存在于外沟Claudius，Boettcher和根细胞中。在螺旋神经节，Reissner膜和血管纹中也发现了低水平的表达。基本通道（KCNJ10和KCNQ1）有助于血管纹状体中K（+）的分泌在Kcnk5（-/-）小鼠中具有正常表达。因此，KCNK5通道对于维持听力是必不可少的。在几种可能的机制中，我们强调了它们在沿外沟侧向路径的K（+）循环中的作用。