| First Author | Haj-Yasein NN | Year | 2011 |
| Journal | Glia | Volume | 59 |
| Issue | 11 | Pages | 1635-42 |
| PubMed ID | 21748805 | Mgi Jnum | J:175546 |
| Mgi Id | MGI:5286008 | Doi | 10.1002/glia.21205 |
| Citation | Haj-Yasein NN, et al. (2011) Evidence that compromised K(+) spatial buffering contributes to the epileptogenic effect of mutations in the human kir4.1 gene (KCNJ10). Glia 59(11):1635-42 |
| abstractText | 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. |
