中国神经再生研究(英文版) ›› 2018, Vol. 13 ›› Issue (4): 651-652.doi: 10.4103/1673-5374.230355

• 观点:脑损伤修复保护与再生 • 上一篇    下一篇

星形胶质细胞Kir4.1钾通道是否可以作为癫痫和心境障碍的新型治疗靶点?

  

  • 收稿日期:2018-03-12 出版日期:2018-04-15 发布日期:2018-04-15

Astrocytic Kir4.1 potassium channels as a novel therapeutic target for epilepsy and mood disorders

Yukihiro Ohno   

  1. Laboratory of Pharmacology, Osaka University of Pharmaceutical Sciences, Osaka, Japan
  • Received:2018-03-12 Online:2018-04-15 Published:2018-04-15
  • Contact: Yukihiro Ohno, Ph.D., yohno@gly.oups.ac.jp.
  • Supported by:

    This work was supported in part by a Grant from AMED (17ek0109120h0003) and by a Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology (17K08324 and 15H04892).

摘要:

orcid: 0000-0001-5349-7135 (Yukihiro Ohno)

Abstract:

Astrocytic Kir4.1 channels and spatial potassium buffering: Astrocytes play a crucial role in maintaining the structural and functional integrity of the brain, which includes formation of the blood-brain barrier, maintenance of water and ion homeostasis, metabolism of neurotransmitters and secretion of various neuroactive molecules. Among these functions, spatial potassium (K+) buffering by astrocytes is an essential system for controlling extracellular K+ concentration ([K+]o) and neuronal . Neurons normally release considerable amounts of K+ during the repolarization phase of an action potential. At tripartite synapses, a single action potential elevates the local [K+]o level by about 1 mM and, if uncorrected, [K+]o reaches 10 mM or more, causing abnormal discharges and finally spreading depression.Spatial K+ buffering by astrocytes is a K+-clearance system which removes an excess of extracellular K+ and transports it to the regions of low [K+]o such as capillary vessels . In addition,the spatial K+ buffering system is coupled to astrocytic glutamate uptake by glutamate transporters (e.g., EAAT1 and EAAT2) and water transport by aquaporin-4 (AQP4)