help button home button Am J Pathol Angiogenesis Meeting
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Dixon, R. W.
Right arrow Articles by Harris, J. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dixon, R. W.
Right arrow Articles by Harris, J. B.
(American Journal of Pathology. 1999;154:447-455.)
© 1999 American Society for Investigative Pathology

Regular Articles

Nerve Terminal Damage by ß-Bungarotoxin

Its Clinical Significance

Rupert W. Dixon and John B. Harris

From the School of Neurosciences and Psychiatry, Department of Neurobiology, Medical School, University of Newcastle upon Tyne, Newcastle upon Tyne, United Kingdom

We report here original data on the biological basis of prolonged neuromuscular paralysis caused by the toxic phospholipase A2 ß-bungarotoxin. Electron microscopy and immunocytochemical labeling with anti-synaptophysin and anti-neurofilament have been used to show that the early onset of paralysis is associated with the depletion of synaptic vesicles from the motor nerve terminals of skeletal muscle and that this is followed by the destruction of the motor nerve terminal and the degeneration of the cytoskeleton of the intramuscular axons. The postjunctional architecture of the junctions were unaffected and the binding of fluorescein-isothiocyanate-conjugated {alpha}-bungarotoxin to achetylcholine receptor was not apparently affected by exposure to ß-bungarotoxin. The re-innervation of the muscle fiber was associated by extensive pre- and post-terminal sprouting at 3 to 5 days but was stable by 7 days. Extensive collateral innervation of adjacent muscle fibers was a significant feature of the re-innervated neuromuscular junctions. These findings suggest that the prolonged and severe paralysis seen in victims of envenoming bites by kraits (elapid snakes of the genus Bungarus) and other related snakes of the family Elapidae is caused by the de-pletion of synaptic vesicles from motor nerve terminals and the degeneration of the motor nerve terminal and intramuscular axons.




This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
M. Rigoni, P. Pizzo, G. Schiavo, A. E. Weston, G. Zatti, P. Caccin, O. Rossetto, T. Pozzan, and C. Montecucco
Calcium Influx and Mitochondrial Alterations at Synapses Exposed to Snake Neurotoxins or Their Phospholipid Hydrolysis Products
J. Biol. Chem., April 13, 2007; 282(15): 11238 - 11245.
[Abstract] [Full Text] [PDF]

Home page
 BrainHome page
S. Prasarnpun, J. Walsh, S. S. Awad, and J. B. Harris
Envenoming bites by kraits: the biological basis of treatment-resistant neuromuscular paralysis
Brain, December 1, 2005; 128(12): 2987 - 2996.
[Abstract] [Full Text] [PDF]

Home page
 BrainHome page
G. M. O'Hanlon, J. J. Plomp, M. Chakrabarti, I. Morrison, E. R. Wagner, C. S. Goodyear, X. Yin, B. D. T. Trapp, J. Conner, P. C. Molenaar, et al.
Anti-GQ1b ganglioside antibodies mediate complement-dependent destruction of the motor nerve terminal
Brain, May 1, 2001; 124(5): 893 - 906.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1999 by the American Society for Investigative Pathology.