Control of K(Ca) channels by calcium nano/microdomains

Neuron. 2008 Sep 25;59(6):873-81. doi: 10.1016/j.neuron.2008.09.001.


Transient elevations in cytoplasmic Ca(2+) trigger a multitude of Ca(2+)-dependent processes in CNS neurons and many other cell types. The specificity, speed, and reliability of these processes is achieved and ensured by tightly restricting Ca(2+) signals to very local spatiotemporal domains, "Ca(2+) nano- and microdomains," that are centered around Ca(2+)-permeable channels. This arrangement requires that the Ca(2+)-dependent effectors reside within these spatial boundaries where the properties of the Ca(2+) domain and the Ca(2+) sensor of the effector determine the channel-effector activity. We use Ca(2+)-activated K(+) channels (K(Ca)) with either micromolar (BK(Ca) channels) or submicromolar (SK(Ca) channels) affinity for Ca(2+) ions to provide distance constraints for Ca(2+)-effector coupling in local Ca(2+) domains and review their significance for the cell physiology of K(Ca) channels in the CNS. The results may serve as a model for other processes operated by local Ca(2+) domains.

Publication types

  • Review

MeSH terms

  • Animals
  • Calcium / physiology*
  • Calcium Signaling / physiology*
  • Central Nervous System / cytology
  • Central Nervous System / physiology
  • Cytoplasm / metabolism
  • Humans
  • Membrane Microdomains / physiology*
  • Neurons / metabolism
  • Potassium Channels, Calcium-Activated / metabolism*
  • Second Messenger Systems / physiology*


  • Potassium Channels, Calcium-Activated
  • Calcium