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The mechanism underlying maintenance of the endocochlear potential by the K+ transport system in fibrocytes of the inner ear

机译:K +转运系统维持内耳纤维细胞内耳蜗电位的潜在机制

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摘要

The endocochlear potential (EP) of +80 mV in the scala media, which is indispensable for audition, is controlled by K+ transport across the lateral cochlear wall. This wall includes two epithelial barriers, the syncytium and the marginal cells. The former contains multiple cell types, such as fibrocytes, which are exposed to perilymph on their basolateral surfaces. The apical surfaces of the marginal cells face endolymph. Between the two barriers lies the intrastrial space (IS), an extracellular space with a low K+ concentration ([K+]) and a potential similar to the EP. This intrastrial potential (ISP) dominates the EP and represents the sum of the diffusion potential elicited by a large K+ gradient across the apical surface of the syncytium and the syncytium's potential, which is slightly positive relative to perilymph. Although a K+ transport system in fibrocytes seems to contribute to the EP, the mechanism remains uncertain. We examined the electrochemical properties of the lateral wall of guinea pigs with electrodes sensitive to potential and K+ while perfusing into the perilymph of the scala tympani blockers of Na+,K+-ATPase, the K+ pump thought to be essential to the system. Inhibiting Na+,K+-ATPase barely affected [K+] in the IS but greatly decreased [K+] within the syncytium, reducing the K+ gradient across its apical surface. The treatment hyperpolarized the syncytium only moderately. Consequently, both the ISP and the EP declined. Fibrocytes evidently use the Na+,K+-ATPase to achieve local K+ transport, maintaining the syncytium's high [K+] that is crucial for the K+ diffusion underlying the positive ISP.
机译:ala骨介质中+80 mV的耳蜗内电势(EP)是听觉必不可少的,它受跨侧耳蜗壁的K + 转运的控制。该壁包括两个上皮屏障,合胞体和边缘细胞。前者包含多种细胞类型,例如纤维细胞,它们在基底外侧表面暴露于淋巴。边缘细胞的顶表面面对内淋巴。在两个障碍之间是内膜间隙(IS),低K + 浓度([K + ])和类似于EP的电位的细胞外空间。纹状体内电位(ISP)支配着EP,代表跨合体顶表面大K + 梯度引起的扩散电位与合胞体电位的总和,相对于周围淋巴,该电位略为正。尽管纤维细胞中的K + 转运系统似乎对EP起作用,但其机制仍不确定。我们检查了对电位和K + 敏感的电极,同时向Na + ,K < sup> + -ATPase,K + 泵被认为对系统至关重要。抑制Na + ,K + -ATPase对IS中的[K + ]几乎没有影响,但大大降低了[K + ] >]在合胞体中,可减小其顶端表面的K + 梯度。治疗仅使合胞体超极化。因此,ISP和EP均下降。纤维细胞显然使用Na + ,K + -ATPase来实现局部K + 转运,从而保持合胞体的高[K + < / sup>]对于正ISP的K + 扩散至关重要。

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