Add time:08/27/2019         Source:sciencedirect.com

The neurotoxic phospholipase A2, β-bungarotoxin, caused the failure of the mechanical response of the indirectly stimulated rat diaphragm. Exposure to β-bungarotoxin had no effect on the response of the muscle to direct stimulation. Resting membrane potentials of muscle fibres exposed to the toxin were similar to control values, and the binding of FITC-labelled α-bungarotoxin to nAChR at the neuromuscular junction was unchanged. Motor nerve terminal boutons at a third of cell junctions were destroyed by exposure to β-bungarotoxin leaving only a synaptic gutter filled with Schwann cell processes and debris. At other junctions, some or all boutons survived exposure to the toxin. Synaptic vesicle density in surviving terminal boutons was reduced by 80% and synaptophysin immunoreactivity by >60% in preparations exposed to β-bungarotoxin, but syntaxin and SNAP-25 immunoreactivity was largely unchanged. Terminal bouton area was also unchanged. The depletion of synaptic vesicles was completely prevented by prior exposure to botulinum toxin C and significantly reduced by prior exposure to conotoxin ω-MVIIC. The data suggest that synaptic vesicle depletion is caused primarily by a toxin-induced entry of Ca2+ into motor nerve terminals via voltage gated Ca2+ channels and an enhanced exocytosis via the formation of t- and v-SNARE complexes.

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