钾离子循环与内淋巴电位
K+ cycling and the endocochlear potential.
作者信息
Wangemann Philine
机构信息
Cell Physiology Laboratory, Anatomy and Physiology Department, Kansas State University, 1600 Denison Avenue, Manhattan 66506, USA.
出版信息
Hear Res. 2002 Mar;165(1-2):1-9. doi: 10.1016/s0378-5955(02)00279-4.
Sensory transduction in the cochlea and the vestibular labyrinth depends on the cycling of K+. In the cochlea, endolymphatic K+ flows into the sensory hair cells via the apical transduction channel and is released from the hair cells into perilymph via basolateral K+ channels including KCNQ4. K+ may be taken up by fibrocytes in the spiral ligament and transported from cell to cell via gap junctions into strial intermediate cells. Gap junctions may include GJB2, GJB3 and GJB6. K+ is released from the intermediate cells into the intrastrial space via the KCNJ10 K+ channel that generates the endocochlear potential. From the intrastrial space, K+ is taken up across the basolateral membrane of strial marginal cells via the Na+/2Cl-/K+ cotransporter SLC12A2 and the Na+/K+-ATPase ATP1A1/ATP1B2. Strial marginal cells secrete K+ across the apical membrane into endolymph via the K+ channel KCNQ1/KCNE1, which concludes the cochlear cycle. A similar K+ cycle exists in the vestibular labyrinth. Endolymphatic K+ flows into the sensory hair cells via the apical transduction channel and is released from the hair cells via basolateral K+ channels including KCNQ4. Fibrocytes connected by gap junctions including GJB2 may be involved in delivering K+ to vestibular dark cells. Extracellular K+ is taken up into vestibular dark cells via SLC12A2 and ATP1A1/ATP1B2 and released into endolymph via KCNQ1/KCNE1, which concludes the vestibular cycle. The importance of K+ cycling is underscored by the fact that mutations of KCNQ1, KCNE1, KCNQ4, GJB2, GJB3 and GJB6 lead to deafness in humans and that null mutations of KCNQ1, KCNE1, KCNJ10 and SLC12A2 lead to deafness in mouse models.
耳蜗和前庭迷路中的感觉转导依赖于钾离子（K⁺）的循环。在耳蜗中，内淋巴中的K⁺通过顶端转导通道流入感觉毛细胞，并通过包括KCNQ4在内的基底外侧K⁺通道从毛细胞释放到外淋巴中。K⁺可能被螺旋韧带中的纤维细胞摄取，并通过缝隙连接在细胞间转运到血管纹中间细胞。缝隙连接可能包括GJB2、GJB3和GJB6。K⁺通过产生内淋巴电位的KCNJ10 K⁺通道从中间细胞释放到血管纹内间隙。在血管纹内间隙，K⁺通过Na⁺/2Cl⁻/K⁺协同转运蛋白SLC12A2和Na⁺/K⁺-ATP酶ATP1A1/ATP1B2穿过血管纹边缘细胞的基底外侧膜被摄取。血管纹边缘细胞通过K⁺通道KCNQ1/KCNE1将K⁺跨顶端膜分泌到内淋巴中，从而完成耳蜗循环。在前庭迷路中存在类似的K⁺循环。内淋巴中的K⁺通过顶端转导通道流入感觉毛细胞，并通过包括KCNQ4在内的基底外侧K⁺通道从毛细胞释放。通过包括GJB2在内的缝隙连接相连的纤维细胞可能参与将K⁺传递给前庭暗细胞。细胞外K⁺通过SLC12A2和ATP1A1/ATP1B2被摄取到前庭暗细胞中，并通过KCNQ1/KCNE1释放到内淋巴中，从而完成前庭循环。KCNQ1、KCNE1、KCNQ4、GJB2、GJB3和GJB6的突变会导致人类耳聋，而KCNQ1、KCNE1、KCNJ10和SLC12A2的无效突变会导致小鼠模型耳聋，这一事实强调了K⁺循环的重要性。
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