Ultrastructure of the inner ear of NKCC1-deficient mice
Ultrastructure of the inner ear of NKCC1-deficient mice
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DOI：
10.1016/s0378-5955(01)00263-5
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发表时间：
2001-06-01
期刊：
影响因子：
2.8
通讯作者：
Henson, MM
中科院分区：
文献类型：
--
作者：
Pace, AJ;Madden, VJ;Henson, MM
听觉信号的传导依赖于内耳内离子的流动。我们产生了缺乏NKCC1的小鼠，NKCC1是一种离子共转运体，被认为参与了审判边缘细胞分泌K+。内耳组织学显示部分或几乎全部中膜缺失和雷氏膜塌陷。超微结构分析表明，雷氏膜由3-4层细胞组成，而不是通常的两层，雷氏膜和下层结构之间存在一种未知成分的物质。在Corti隧道内，毛细胞和支持细胞难以识别。被膜位置改变，周围有沉淀。牙间细胞和Boettcher细胞存在严重的结构缺陷，血管纹和II型和IV型纤维细胞存在轻微缺陷。研究发现，主要缺陷主要发生在不表达NKCC1的细胞中，这表明NKCC1的缺失会导致表达NKCC1的细胞出现功能缺陷，并对K+再循环途径下游的细胞群体产生形态学影响。(C) 2001 Elsevier Science B.V.版权所有
The transduction of the auditory signal is dependent on the flow of ions within the inner ear. We have generated mice deficient in NKCC1, an ion cotransporter that is thought to be involved in the secretion of K+ by the strial marginal cells. Inner ear histology revealed partial to almost total absence of the scala media and collapse of Reissner's membrane. Ultrastructural analysis showed that Reissner's membrane consists of 3-4 cell layers instead of the usual two, and a substance of unknown composition is present between Reissner's membrane and underlying structures. Within the tunnel of Corti, hair cells and supporting cells were difficult to identify. The location of the tectorial membrane was altered, and a precipitate was observed surrounding it. Severe structural defects were noted in the interdental cells and Boettcher cells, and mild defects were observed in the stria vascularis and in type II and type IV fibrocytes. The finding that major defects occur predominantly in cells that are not known to express NKCC1 suggests that loss of NKCC1 results in functional defects in cells expressing NKCC1 and a morphological effect on cell populations downstream in the proposed K+ recycling pathway. (C) 2001 Elsevier Science B.V. All rights reserved.