Weber P C, Cunningham C D, Schulte B A
Department of Otolaryngology-Head and Neck Surgery, Medical University of South Carolina, Charleston, South Carolina 29425, USA.
Laryngoscope. 2001 Jul;111(7):1156-65. doi: 10.1097/00005537-200107000-00006.
OBJECTIVES/HYPOTHESIS: Potential pathways for recycling potassium (K+) used in the maintenance of inner ear electrochemical gradients have been elucidated in animal models. However, little is known about K+ transport in the human cochlea. This study was designed to characterize putative K+ recycling pathways in the human ear and to determine whether observations from animal models can be extrapolated to humans.
A prospective laboratory study using an immunohistochemical approach to analyze the distribution of key ion transport mediators in the human cochlea.
Human temporal bones were fixed in situ within 1 to 6 hours of death and subsequently harvested at autopsy. Decalcification was accomplished with the aid of microwaving. Immunohistochemical staining was then performed to define the presence and cell type-specific distribution of Na,K-ATPase, sodium-potassium-chloride cotransporter (NKCC), and carbonic anhydrase (CA) in the inner ear.
Staining patterns visualized in the human cochlea closely paralleled those seen in other species. Anti-Na,K-ATPase stained strongly the basolateral plasma membrane of strial marginal cells and nerve endings underlying hair cells. This antibody also localized Na,K-ATPase to type II, type IV, and type V fibrocytes in the spiral ligament and in limbal fibrocytes. NKCC was present in the basolateral membrane of strial marginal cells as well as in type II, type V, and limbal fibrocytes. Immunoreactive carbonic anhydrase was present in type I and type III fibrocytes and in epithelial cells lining Reissner's membrane and the spiral prominence.
The distribution of several major ion transport proteins in the human cochlea is similar but not identical to that described in various rodent models. These results support the presence of a complex system for recycling and regulating K+ homeostasis in the human cochlea, similar to that described in other mammalian species.
目的/假设：动物模型已阐明了用于维持内耳电化学梯度的钾离子（K+）循环利用的潜在途径。然而，关于人耳蜗中K+转运的情况却知之甚少。本研究旨在描述人耳中假定的K+循环途径，并确定能否将动物模型中的观察结果外推至人类。
一项前瞻性实验室研究，采用免疫组织化学方法分析人耳蜗中关键离子转运介质的分布。
人颞骨在死亡后1至6小时内原位固定，随后在尸检时采集。借助微波进行脱钙。然后进行免疫组织化学染色，以确定内耳中钠钾ATP酶、钠钾氯协同转运蛋白（NKCC）和碳酸酐酶（CA）的存在及细胞类型特异性分布。
人耳蜗中观察到的染色模式与其他物种中所见的模式极为相似。抗钠钾ATP酶抗体强烈染色血管纹边缘细胞的基底外侧质膜以及毛细胞下方的神经末梢。该抗体还将钠钾ATP酶定位到螺旋韧带中的II型、IV型和V型纤维细胞以及边缘纤维细胞中。NKCC存在于血管纹边缘细胞的基底外侧膜以及II型、V型和边缘纤维细胞中。免疫反应性碳酸酐酶存在于I型和III型纤维细胞以及覆盖Reissner膜和螺旋隆起的上皮细胞中。
人耳蜗中几种主要离子转运蛋白的分布与各种啮齿动物模型中描述的相似但不完全相同。这些结果支持人耳蜗中存在一个类似于其他哺乳动物物种中所描述的用于循环利用和调节K+稳态的复杂系统。
