Potassium Homeostasis in Glia

Research output: Chapter in Book/Report/Conference proceedingChapter

3 Scopus citations

Abstract

Diverse cellular mechanisms exist in the central nervous system to counteract rapid changes in extracellular K+ concentration that occur with neuronal activity. These mechanisms of K+ buffering include net K+ uptake into glial cells and K+ spatial buffering by glia. With net K+ uptake, K+ influx into glial cells occurs via activity of the Na, K-ATPase pump and by ion flux through Na–K–Cl cotransporters. With K+ spatial buffering, regulation of local K+ changes occurs by a K+ current flow through glial cells, transferring K+ from areas of high concentration to areas of low concentration. A specialized form of K+ spatial buffering, termed K+ siphoning, occurs in the retina, where K+ currents are directed preferentially through cell end feet.

Original languageEnglish (US)
Title of host publicationEncyclopedia of Neuroscience
Subtitle of host publicationVolumes 1-11
PublisherElsevier
PagesV8-867-V8-872
Number of pages6
Volume8
ISBN (Electronic)9780080450469
ISBN (Print)9780080446172
DOIs
StatePublished - Jan 1 2009

Bibliographical note

Publisher Copyright:
© 2009 Elsevier Ltd. All rights reserved.

Keywords

  • Aquaporin
  • Astrocytes
  • Connexins
  • Glia
  • Inwardly rectifying potassium channel
  • Kir4.1
  • Müller cells
  • Potassium
  • Potassium buffering
  • Potassium channel
  • Potassium siphoning
  • Potassium spatial buffering
  • Retina
  • Sodium pump

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