Astrocyte Kir4.1 ion channel deficits contribute to neuronal dysfunction in Huntington's disease model mice

被引：0
|
作者：
Xiaoping Tong
Yan Ao
Guido C Faas
Sinifunanya E Nwaobi
Ji Xu
Martin D Haustein
Mark A Anderson
Istvan Mody
Michelle L Olsen
Michael V Sofroniew
Baljit S Khakh
机构：
[1] David Geffen School of Medicine,Department of Physiology
[2] University of California Los Angeles,Department of Neurobiology
[3] David Geffen School of Medicine,Department of Neurology
[4] University of California Los Angeles,Department of Cell
[5] David Geffen School of Medicine,undefined
[6] University of California Los Angeles,undefined
[7] Developmental and Integrative Biology,undefined
[8] University of Alabama at Birmingham,undefined
来源：
Nature Neuroscience | 2014年 / 17卷
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摘要：
In this study, the authors show that altered medium spiny neuron excitability and symptom onset in Huntington's disease model mice is associated with decreased expression of Kir4.1 and impaired K+ handling by astrocytes. Exogenous expression of Kir4.1 could partially rescue motor function and prolong survival in HD mice.
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页码：694 / 703
页数：9
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