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

关键词：

D O I：

暂无

中图分类号：

学科分类号：

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.

引用

页码：694 / 703

页数：9

共 28 条

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