In:
Glia, Wiley, Vol. 59, No. 11 ( 2011-11), p. 1635-1642
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. © 2011 Wiley‐Liss, Inc.
Type of Medium:
Online Resource
ISSN:
0894-1491
,
1098-1136
Language:
English
Publisher:
Wiley
Publication Date:
2011
detail.hit.zdb_id:
1474828-9
SSG:
12
