The Journal of Neurophysiology Vol. 85 No. 5 May 2001, pp. 1952-1959
Copyright ©2001 by the American Physiological Society

Extracellular Calcium Depletion as a Mechanism of Short-Term Synaptic Depression

Center for Theoretical Neuroscience, Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030

King, Richard D., Michael C. Wiest, and P. Read Montague. Extracellular Calcium Depletion as a Mechanism of Short-Term Synaptic Depression. J. Neurophysiol. 85: 1952-1959, 2001. 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.