Immunogold evidence suggests that coupling of K+ siphoning and water transport in rat retinal Müller cells is mediated by a coenrichment of Kir4.1 and AQP4 in specific membrane domains
Article first published online: 26 FEB 1999
Copyright © 1999 Wiley-Liss, Inc.
Volume 26, Issue 1, pages 47–54, March 1999
How to Cite
Nagelhus, E. A., Horio, Y., Inanobe, A., Fujita, A., Haug, F.-m., Nielsen, S., Kurachi, Y. and Ottersen, O. P. (1999), Immunogold evidence suggests that coupling of K+ siphoning and water transport in rat retinal Müller cells is mediated by a coenrichment of Kir4.1 and AQP4 in specific membrane domains. Glia, 26: 47–54. doi: 10.1002/(SICI)1098-1136(199903)26:1<47::AID-GLIA5>3.0.CO;2-5
- Issue published online: 26 FEB 1999
- Article first published online: 26 FEB 1999
- Manuscript Accepted: 29 SEP 1998
- Manuscript Received: 31 AUG 1998
- Norwegian Research Council
- Letten F. Saugstad's Fund
- European Union Biomed Programme. Grant Number: PL962118
- water homeostasis;
- potassium buffering;
Postembedding immunogold labeling was used to examine the subcellular distribution of the inwardly rectifying K+ channel Kir4.1 in rat retinal Müller cells and to compare this with the distribution of the water channel aquaporin-4 (AQP4). The quantitative analysis suggested that both molecules are enriched in those plasma membrane domains that face the vitreous body and blood vessels. In addition, Kir4.1, but not AQP4, was concentrated in the basal ∼300–400 nm of the Müller cell microvilli. These data indicate that AQP4 may mediate the water flux known to be associated with K+ siphoning in the retina. By its highly differentiated distribution of AQP4, the Müller cell may be able to direct the water flux to select extracellular compartments while protecting others (the subretinal space) from inappropriate volume changes. The identification of specialized membrane domains with high Kir4.1 expression provides a morphological correlate for the heterogeneous K+ conductance along the Müller cell surface. GLIA 26:47–54, 1999. © 1999 Wiley-Liss, Inc.