Evidence that compromised K+ spatial buffering contributes to the epileptogenic effect of mutations in the human kir4.1 gene (KCNJ10)
Article first published online: 11 JUL 2011
Copyright © 2011 Wiley-Liss, Inc.
Volume 59, Issue 11, pages 1635–1642, November 2011
How to Cite
Haj-Yasein, N. N., Jensen, V., Vindedal, G. F., Gundersen, G. A., Klungland, A., Ottersen, O. P., Hvalby, Ø. and Nagelhus, E. A. (2011), Evidence that compromised K+ spatial buffering contributes to the epileptogenic effect of mutations in the human kir4.1 gene (KCNJ10). Glia, 59: 1635–1642. doi: 10.1002/glia.21205
- Issue published online: 14 SEP 2011
- Article first published online: 11 JUL 2011
- Manuscript Accepted: 1 JUN 2011
- Manuscript Revised: 27 MAY 2011
- Manuscript Received: 21 FEB 2011
- Research Council of Norway and Letten Foundation
- Polish-Norwegian Research Fund. Grant Number: PNRF-96
- K+ buffering;
Mutations in the human Kir4.1 potassium channel gene (KCNJ10) are associated with epilepsy. Using a mouse model with glia-specific deletion of Kcnj10, we have explored the mechanistic underpinning of the epilepsy phenotype. The gene deletion was shown to delay K+ clearance after synaptic activation in stratum radiatum of hippocampal slices. The activity-dependent changes in extracellular space volume did not differ between Kcnj10 mutant and wild-type mice, indicating that the Kcnj10 gene product Kir4.1 mediates osmotically neutral K+ clearance. Combined, our K+ and extracellular volume recordings indicate that compromised K+ spatial buffering in brain underlies the epilepsy phenotype associated with human KCNJ10 mutations. © 2011 Wiley-Liss, Inc.