| First Author | Song F | Year | 2018 |
| Journal | Commun Biol | Volume | 1 |
| Pages | 80 | PubMed ID | 30271961 |
| Mgi Jnum | J:278523 | Mgi Id | MGI:6356262 |
| Doi | 10.1038/s42003-018-0083-x | Citation | Song F, et al. (2018) Kir4.1 channels in NG2-glia play a role in development, potassium signaling, and ischemia-related myelin loss. Commun Biol 1:80 |
| abstractText | 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. |
