Referenced in: none

Automatically associated channels: Kir1.1 , Kir4.1

Title: Evidence that compromised K+ spatial buffering contributes to the epileptogenic effect of mutations in the human Kir4.1 gene (KCNJ10).

Authors: Nadia Nabil Haj-Yasein, Vidar Jensen, Gry Fluge Vindedal, Georg Andreas Gundersen, Arne Klungland, Ole Petter Ottersen, Oivind Hvalby, Erlend Arnulf Nagelhus

Journal, date & volume: Glia, 2011 Nov , 59, 1635-42

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/21748805

Abstract
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.