Toggle Main Menu Toggle Search

Open Access padlockePrints

β-bungarotoxin-induced depletion of synaptic vesicles at the mammalian neuromuscular junction

Lookup NU author(s): Surisak Prasarnpun, Emeritus Professor John Harris


Full text for this publication is not currently held within this repository. Alternative links are provided below where available.


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 Ca 2+ channels and an enhanced exocytosis via the formation of t- and v-SNARE complexes. © 2004 Elsevier Ltd. All rights reserved.

Publication metadata

Author(s): Prasarnpun S, Walsh J, Harris JB

Publication type: Article

Publication status: Published

Journal: Neuropharmacology

Year: 2004

Volume: 47

Issue: 2

Pages: 304-314

Print publication date: 01/08/2004

ISSN (print): 0028-3908

ISSN (electronic): 1873-7064

Publisher: Pergamon


DOI: 10.1016/j.neuropharm.2004.04.012

PubMed id: 15223309


Altmetrics provided by Altmetric