Extracellular calcium depletion in synaptic transmission

Neuroscientist. 2004 Feb;10(1):12-7. doi: 10.1177/1073858403259440.


Regulation of Ca2+ homeostasis in the extracellular space plays an important role in neuronal function. Several modeling studies and recent measurements have demonstrated that modest action potential or synaptic activity can result in a significant reduction in extracellular calcium ([Ca]o(2+)). Changes in [Ca]o(2+) can regulate intracellular signaling enzymes, such as Ca2+/calmodulin-dependent protein kinase II, and influence neuronal function at synaptic and nonsynaptic sites. The change in [Ca]o(2+) can affect several types of ion channels and neurotransmitter receptors and activate a Ca(2+)-sensitive receptor in neuronal membranes. Depletion of [Ca]o(2+) may function as an activity-dependent extracellular messenger that regulates nervous system function during development, learning, and disease.

Publication types

  • Review

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Extracellular Fluid / metabolism*
  • Humans
  • Receptors, G-Protein-Coupled / chemistry
  • Receptors, G-Protein-Coupled / metabolism
  • Synaptic Transmission / physiology*


  • Receptors, G-Protein-Coupled
  • Calcium