Residual Ca^{2 +} and short-term synaptic plasticity

Abstract

AT many synapses, the amount of transmitter released by action potentials increases progressively during a train of spikes. This enhancement of evoked transmitter release grows during tetanic stimulation with several time constants, each bearing a different name (facilitation: tens to hundreds of milliseconds; augmentation: several seconds; potentiation: several minutes), and the enhance-ment of release to test spikes after a tetanus decays with similar time constants. All these processes depend on presynaptic Ca^{2 +} influx during the conditioning tetanus¹. It has often been proposed that these forms of synaptic plasticity are due to residual Ca^{2 +} present in nerve terminals following conditioning activity². We tested this idea directly by using photolabile Ca^{2 +} chelators to reduce residual Ca2 * following conditioning stimulation or to gen-erate an artificial elevation in Ca^{2 +} concentration, and observed the effects on synaptic transmission at crayfish neuromuscular junctions. We found that facilitation, augmentation and potentia-tion are caused by the continuing action of residual Ca^{2 +}. Augmen-tation and potentiation seem to arise from Ca^{2 +} acting at a separate site from facilitation, and these sites are different from the molecular target triggering neurosecretion.