KCNJ10 (Kir4.1) potassium channel knockout abolishes endocochlear potential
KCNJ10 (Kir4.1) potassium channel knockout abolishes endocochlear potential
复制标题
DOI：
10.1152/ajpcell.00312.2001
复制
发表时间：
2002-02-01
影响因子：
5.5
通讯作者：
Kofuji, P
中科院分区：
文献类型：
--
作者：
Marcus, DC;Wu, T;Kofuji, P
耳蜗纹的血管纹产生耳蜗内电势并分泌K+，K+是主要的电荷载体，耳蜗内电势是导致听力的感觉传导的主要驱动力。血管纹由两个屏障组成，即分泌钾的边缘细胞和通过缝隙连接与中间细胞相连的基底细胞。在STATE中间细胞中缺乏KCNJ10(Kir4.1)K+通道的小鼠不会产生耳蜗内电位。内淋巴体积和K+浓度([K+])降低。这些研究表明，KCNJ10 K+通道提供了产生耳蜗内电位的分子机制，并与其他跨通道建立[K+]差异的运输途径相协调。KCNJ10也是K+分泌的限制途径。
Stria vascularis of the cochlea generates the endocochlear potential and secretes K+.K+ is the main charge carrier and the endocochlear potential the main driving force for the sensory transduction that leads to hearing. Stria vascularis consists of two barriers, marginal cells that secrete potassium and basal cells that are coupled via gap junctions to intermediate cells. Mice lacking the KCNJ10 (Kir4.1) K+ channel in strial intermediate cells did not generate an endocochlear potential. Endolymph volume and K+ concentration ([K+]) were reduced. These studies establish that the KCNJ10 K+ channel provides the molecular mechanism for generation of the endocochlear potential in concert with other transport pathways that establish the [K+] difference across the channel. KCNJ10 is also a limiting pathway for K+ secretion.