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Mechanisms of calcium sequestration during facilitation at active zones of an amphibian neuromuscular junction
Authors:Bennett M R  Farnell L  Gibson W G  Dickens P
Institution:The Neurobiology Laboratory, Department of Physiology, The Institute for Biomedical Research, University of Sydney, New South Wales 2006, Australia. maxb@physiol.usyd.edu.au
Abstract:The calcium transients (DeltaCa(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 DeltaCa(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 DeltaCa(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.
Keywords:Calcium  Facilitation  Low-affinity calcium indicator  Sequestration  Mitochondria  Endoplasmic reticulum
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