CALCIUM AND SHORT-TERM SYNAPTIC PLASTICITY

The sites of presynaptic action of calcium ions in triggering exocytosis and in activating various forms of short-term enhancement of synaptic transmission are discussed. A detailed presentation of methods and results is left to original publications. Instead, an attempt is made to collate a variety of findings and synthesize a picture of how Ca2+ operates in nerve terminals to trigger release and enhance evoked release following electrical activity. It is concluded that Ca2+ triggers neurosecretion by acting very near Ca2+ channel mouths, at high concentration, with high stoichiometry, to activate low affinity binding sites with fast kenetics. Facilitation, augmentation, and potentiation are consequences of actions of residual presynaptic Ca2+ remaining after prior electrical activity. Facili6tation is caused by Ca2+ acting with fast kinetics, but probably with moderately high affinity al a site distinct from the secretory trigger. Augmentation and potentiation are caused by residual Ca2+ acting at yet another site, probably of high affinity, and with rate constants of about Is. Post-tetanic potentiation lasts so long because nerve terminals cannot remove residual Ca2+ quickly after prolonged stimulation. Processes similar to augmentation and potentiation apear to occur at some hormonal cells as well as in neurons. The molecular receptors for Ca2+ in short-term synaptic plasticity have yet to be identified, but Ca2+/calmodulin protein kinase II is not a likely candidate.