Extracellular calcium depletion as a mechanism of short-term synaptic depression

Richard D. King, Michael C. Wiest, P. Read Montague

Research output: Contribution to journalArticlepeer-review

16 Scopus citations

Abstract

Recent experiments have demonstrated that normal neural activity can cause significant decrements in external calcium levels, and that these decrements mediate a form of short-term synaptic depression. These findings raise the possibility that certain forms of short-term synaptic depression at glutamatergic synapses throughout the mammalian CNS may be influenced by similar changes in external calcium. We use a computational model of the extracellular space, combined with experimental data on calcium consumption, to show that such short-term depression can be accounted for by changes in calcium just outside active synapses, provided that external calcium diffusion is restricted. Remarkably, the model suggests the novel possibility that synapses may possess private pools of external calcium that enforce some forms of short-term depression in a synapse-specific manner.

Original languageEnglish
Pages (from-to)1952-1959
Number of pages8
JournalJournal of Neurophysiology
Volume85
Issue number5
DOIs
StatePublished - 2001

ASJC Scopus subject areas

  • Neuroscience (all)
  • Physiology

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