中国神经再生研究(英文版) ›› 2020, Vol. 15 ›› Issue (6): 980-987.doi: 10.4103/1673-5374.270295

• 综述:神经损伤修复保护与再生 • 上一篇    下一篇

癫痫发作时星形胶质细胞对钾的调节作用

  

  • 出版日期:2020-06-15 发布日期:2020-07-01

Astrocytic modulation of potassium under seizures

Fushun Wang1, 2, Xiaoming Qi1, Jun Zhang3, Jason H. Huang1, 4   

  1. 1 Department of Neurosurgery, Baylor Scott & White Health, Temple, TX, USA
    2 Institute of Brain and Psychological Science, Sichuan Normal University, Chengdu, Sichuan Province, China
    3 Department of Neurosurgery, PLA General Hospital, Beijing, China
    4 Department of Surgery, Texas A&M University College of Medicine, Temple, TX, USA
  • Online:2020-06-15 Published:2020-07-01
  • Contact: Jun Zhang, MD,junzhang301@163.com; Jason H. Huang, MD,jason.huang@bswhealth.org.
  • Supported by:
    This work was supported partially by Helen Vosburg McCrillus Plummer and Robert Edward Lee Plummer, Jr. Chair in Neurosurgery
    (JHH) and by NIH-R01-NS-067435 (to JHH).

摘要: orcid: 0000-0002-4426-0168 (Jason H. Huang)

Abstract: The contribution of an impaired astrocytic K+ regulation system to epileptic neuronal hyperexcitability has been increasingly recognized in the last decade. A defective K+ regulation leads to an elevated extracellular K+ concentration ([K+]o). When [K+]o reaches peaks of 10–12 mM, it is strongly associated with seizure initiation during hypersynchronous neuronal activities. On the other hand, reactive astrocytes during a seizure attack restrict influx of K+ across the membrane both passively and actively. In addition to decreased K+ buffering, aberrant Ca2+ signaling and declined glutamate transport have also been observed in astrogliosis in epileptic specimens, precipitating an increased neuronal discharge and induction of seizures. This review aims to provide an overview of experimental findings that implicated astrocytic modulation of extracellular K+ in the mechanism of epileptogenesis.

Key words: AQP4, Ca2+ signaling, cell volume, connexins, epilepsy, K+ buffering, miRNA, NKCC, pannexin, TBI