Potassium buffering in the central nervous system

Neuroscience. 2004;129(4):1045-56. doi: 10.1016/j.neuroscience.2004.06.008.


Rapid changes in extracellular K+ concentration ([K+](o)) in the mammalian CNS are counteracted by simple passive diffusion as well as by cellular mechanisms of K+ clearance. Buffering of [K+](o) can occur via glial or neuronal uptake of K+ ions through transporters or K+-selective channels. The best studied mechanism for [K+](o) buffering in the brain is called K+ spatial buffering, wherein the glial syncytium disperses local extracellular K+ increases by transferring K+ ions from sites of elevated [K+](o) to those with lower [K+](o). In recent years, K+ spatial buffering has been implicated or directly demonstrated by a variety of experimental approaches including electrophysiological and optical methods. A specialized form of spatial buffering named K+ siphoning takes place in the vertebrate retina, where glial Muller cells express inwardly rectifying K+ channels (Kir channels) positioned in the membrane domains near to the vitreous humor and blood vessels. This highly compartmentalized distribution of Kir channels in retinal glia directs K+ ions from the synaptic layers to the vitreous humor and blood vessels. Here, we review the principal mechanisms of [K+](o) buffering in the CNS and recent molecular studies on the structure and functions of glial Kir channels. We also discuss intriguing new data that suggest a close physical and functional relationship between Kir and water channels in glial cells.

Publication types

  • Review

MeSH terms

  • Animals
  • Aquaporins / metabolism
  • Buffers
  • Cell Membrane / physiology*
  • Central Nervous System / physiology*
  • Humans
  • Neuroglia / cytology
  • Neuroglia / physiology
  • Potassium / metabolism*
  • Potassium Channels / physiology*
  • Retina / cytology
  • Retina / physiology
  • Water-Electrolyte Balance / physiology*


  • Aquaporins
  • Buffers
  • Potassium Channels
  • Potassium