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 language | English (US) |
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Title of host publication | Encyclopedia of Neuroscience |
Subtitle of host publication | Volumes 1-11 |
Publisher | Elsevier |
Pages | V8-867-V8-872 |
Number of pages | 6 |
Volume | 8 |
ISBN (Electronic) | 9780080450469 |
ISBN (Print) | 9780080446172 |
DOIs | |
State | Published - 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