Potassium recycling pathways in the human cochlea.

Published

Journal Article

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. STUDY DESIGN: A prospective laboratory study using an immunohistochemical approach to analyze the distribution of key ion transport mediators in the human cochlea. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Full Text

Duke Authors

Cited Authors

  • Weber, PC; Cunningham, CD; Schulte, BA

Published Date

  • July 2001

Published In

Volume / Issue

  • 111 / 7

Start / End Page

  • 1156 - 1165

PubMed ID

  • 11568535

Pubmed Central ID

  • 11568535

International Standard Serial Number (ISSN)

  • 0023-852X

Digital Object Identifier (DOI)

  • 10.1097/00005537-200107000-00006

Language

  • eng

Conference Location

  • United States