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Kir4.1 channels in NG2-glia play a role in development, potassium signaling, and ischemia-related myelin loss

The contribution of the inwardly rectifying K(+) channel subtype Kir4.1 has been focused mainly on astrocytes, where they play important roles in the maintenance of resting membrane potential, extracellular K(+) uptake, and facilitation of glutamate uptake in the central nervous system. Here, we rep...

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Detalles Bibliográficos
Autores principales: Song, Feier, Hong, Xiaoqi, Cao, Jiayu, Ma, Guofen, Han, Yanfei, Cepeda, Carlos, Kang, Zizhen, Xu, Tianle, Duan, Shumin, Wan, Jieqing, Tong, Xiaoping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6123808/
https://www.ncbi.nlm.nih.gov/pubmed/30271961
http://dx.doi.org/10.1038/s42003-018-0083-x
Descripción
Sumario:The contribution of the inwardly rectifying K(+) channel subtype Kir4.1 has been focused mainly on astrocytes, where they play important roles in the maintenance of resting membrane potential, extracellular K(+) uptake, and facilitation of glutamate uptake in the central nervous system. Here, we report the role of Kir4.1 channels in NG2-glia during brain development, potassium signaling, and in an ischemic stroke disease model. Kir4.1 channels are widely expressed in NG2-glia during brain development. In the adult mouse hippocampus, Kir4.1 channels in NG2-glia constitute more than 80% of K(+) channels inward currents. This large portion of Kir4.1 channel currents exhibits a deficit in NG2-glia as an initial response in a transient ischemic mouse model. Further evidence indicates that Kir4.1 deficits in NG2-glia potentially cause axonal myelin loss in ischemia through the association with oligodendrocyte-specific protein (OSP/Claudin-11), which unravels a potential therapeutic target in the treatment of ischemic stroke.