期刊
GLIA
卷 59, 期 11, 页码 1635-1642出版社
WILEY-BLACKWELL
DOI: 10.1002/glia.21205
关键词
astrocytes; glia; K plus buffering; seizures; epilepsy
资金
- Research Council of Norway and Letten Foundation
- Polish-Norwegian Research Fund [PNRF-96]
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. (C) 2011 Wiley-Liss, Inc.
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