Abstract
The calcium transients ( Δ [ Ca 2 + ] i ) at active zones of amphibian ( Bufo marinus) motor-nerve terminals that accompany impulses, visualized using a low-affinity calcium indicator injected into the terminal, are described and the pathways of subsequent sequestration of the residual calcium determined, allowing development of a quantitative model of the sequestering processes. Blocking the endoplasmic reticulum calcium pump with thapsigargin did not affect Δ [ Ca 2 + ] i for a single impulse but increased its amplitude during short trains. Blocking the uptake of calcium by mitochondria with CCCP had little effect on Δ [ Ca 2 + ] i of a single impulse but greatly increased its amplitude during short trains. This present compartmental model is compatible with our previous Monte Carlo diffusion model of Ca 2 + sequestration during facilitation [Bennett, M.R., Farnell, L., Gibson, W.G., 2004. The facilitated probability of quantal secretion within an array of calcium channels of an active zone at the amphibian neuromuscular junction. Biophys. J. 86(5), 2674–2690], with the single plasmalemma pump in that model now replaced by separate pumps for the plasmalemma and endoplasmic reticulum, as well as the introduction of a mitochondrial uniporter.
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