CALCIUM AND SHORT-TERM SYNAPTIC PLASTICITY

The roles of Ca in phasic transmitter release and short-term synaptic plasticity are reviewed. An action potential evokes phasic release solely by elevating presynaptic Ca concentration locally and briefly to high levels (about 100 mu M) at release sites. Multiple Ca ions bind rapidly to a low affinity site near Ca channels to trigger exocytosis of neurotransmitter-containing vesicles. The localized action of Ca near channel mouths accounts for the lower apparent stoichiometry of Ca action when spikes are broadened or depolarizations increased than when external Ca concentration is increased. At crayfish neuromuscular junctions, several forms of short-term plasticity depend on the action of residual Ca in nerve terminals following conditioning stimulation. Augmentation and potentiation are due to residual Ca acting with slow kinetics (300 ms) at a high affinity site to enhance release to action potentials, while facilitation is due to residual Ca acting at a different site with much faster kinetics. The durations of these processes reflect the time that residual Ca persists at these sites of action after conditioning activity. At mammalian cortical synapses, postsynaptic Ca activates long-term potentiation within a time period of about 2 s.