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J. Biol. Chem., Vol. 279, Issue 27, 28387-28392, July 2, 2004

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The Potassium Channel Kir4.1 Associates with the Dystrophin-Glycoprotein Complex via -Syntrophin in Glia^*

Nathan C. Connors, Marvin E. Adams, Stanley C. Froehner, and Paulo Kofuji¶

From the Department of Neuroscience, University of Minnesota, Minneapolis, Minnesota 55455 and the Department of Physiology and Biophysics, University of Washington, Seattle, Washington 98195

One of the major physiological roles of potassium channels in glial cells is to promote "potassium spatial buffering" in the central nervous system, a process necessary to maintain an optimal potassium concentration in the extracellular environment. This process requires the precise distribution of potassium channels accumulated at high density in discrete subdomains of glial cell membranes. To obtain a better understanding of how glial cells selectively target potassium channels to discrete membrane subdomains, we addressed the question of whether the glial inwardly rectifying potassium channel Kir4.1 associates with the dystrophin-glycoprotein complex (DGC). Immunoprecipitation experiments revealed that Kir4.1 is associated with the DGC in mouse brain and cultured cortical astrocytes. In vitro immunoprecipitation and pull-down assays demonstrated that Kir4.1 can bind directly to -syntrophin, requiring the presence of the last three amino acids of the channel (SNV), a consensus PDZ domain-binding motif. Furthermore, Kir4.1 failed to associate with the DGC in brains from -syntrophin knockout mice. These results suggest that Kir4.1 is localized in glial cells by its association with the DGC through a PDZ domain-mediated interaction with -syntrophin and suggest an important role for the DGC in central nervous system physiology.

Received for publication, March 8, 2004

^* This work was supported by National Institutes of Health Grant EY12949-01 (to P. K.), Vision Training Grant EY07133 (to N. C. C.), and Grant NS33145 (to S. C. F.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^¶ To whom correspondence should be addressed: Dept. of Neuroscience, University of Minnesota, 6-145 Jackson Hall, 321 Church St. SE, Minneapolis, MN 55455. Tel.: 612-625-6457; Fax: 612-626-5009; E-mail: kofuj001{at}tc.umn.edu.

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