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DURING SHORT BURSTS OF NEURONAL ACTIVITY, CHANGES IN THE EFFICACY OF NEUROTRANSMITTER RELEASE ARE GOVERNED PRIMARILY BY TWO COUNTERACTING PROCESSES: (1) Ca(2+)-dependent elevations of vesicle release probability and (2) depletion of synaptic vesicles. The dynamic interplay of both processes contributes to the expression of activity-dependent synaptic plasticity. Here, we exploited various facets of short-term plasticity at the Drosophila neuromuscular junction to dissect these two processes. This enabled us to rigorously analyze different models of synaptic vesicle pools in terms of their size and mobilization properties. Independent of the specific model, we estimate approximately 300 readily releasable vesicles with an average release probability of approximately 50% in 1 mM extracellular calcium ( approximately 5% in 0.4 mM extracellular calcium) under resting conditions. The models also helped interpreting the altered short-term plasticity of the previously reported mutant of the active zone component Bruchpilot (BRP). Finally, our results were independently confirmed through fluctuation analysis. Our data reveal that the altered short-term plasticity observed in BRP mutants cannot be accounted for by delocalized Ca(2+) channels alone and thus suggest an additional role of BRP in short-term plasticity.

Mechanisms of short‐term plasticity at neuromuscular active zones of Drosophila