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. 2011 Nov;59(11):1635-42.
doi: 10.1002/glia.21205. Epub 2011 Jul 11.

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

Nadia Nabil Haj-Yasein  1 , Vidar Jensen, Gry Fluge Vindedal, Georg Andreas Gundersen, Arne Klungland, Ole Petter Ottersen, Oivind Hvalby, Erlend Arnulf Nagelhus
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Evidence that compromised K+ spatial buffering contributes to the epileptogenic effect of mutations in the human Kir4.1 gene (KCNJ10)

Nadia Nabil Haj-Yasein et al. Glia. 2011 Nov.

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.

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