Residual Ca2+ and short-term synaptic plasticity.
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 enhancement of release to test spikes after a tetanus decays with similar time constants. All these processes depend on presynaptic Ca2+ influx during the conditioning tetanus. It has often been proposed that these forms of synaptic plasticity are due to residual Ca2+ present in nerve terminals following conditioning activity. We tested this idea directly by using photolabile Ca2+ chelators to reduce residual Ca2+ following conditioning stimulation or to generate an artificial elevation in Ca2+ concentration, and observed the effects on synaptic transmission at crayfish neuromuscular junctions. We found that facilitation, augmentation and potentiation are caused by the continuing action of residual Ca2+. Augmentation and potentiation seem to arise from Ca2+ acting at a separate site from facilitation, and these sites are different from the molecular target triggering neurosecretion.
Kamiya
H
H
Neurobiology Division, University of California, Berkeley 94720.
Zucker
R S
RS
D000200:Action Potentials; D000818:Animals; D003400:Astacoidea; D002118:Calcium / Q000502:physiology*; D002614:Chelating Agents / Q000494:pharmacology; D003979:Diazonium Compounds; D066298:In Vitro Techniques; D009469:Neuromuscular Junction / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D010642:Phenoxyacetates; D010782:Photolysis; D013569:Synapses / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D014466:Ultraviolet Rays
D002614:Chelating Agents; D003979:Diazonium Compounds; D010642:Phenoxyacetates; C063685:diazo-2; D002118:Calcium