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Brain Advance Access originally published online on September 29, 2005
Brain 2005 128(12):2987-2996; doi:10.1093/brain/awh642
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© The Author (2005). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Envenoming bites by kraits: the biological basis of treatment-resistant neuromuscular paralysis

S. Prasarnpun1, J. Walsh, S. S. Awad and J. B. Harris

School of Neurology, Neurobiology and Psychiatry, Faculty of Medical Sciences, University of Newcastle upon Tyne, Newcastle upon Tyne, UK 1 Present address: Department of Biology, Naresuan University, Phitsanulok 65000, Thailand

Correspondence to: J. B. Harris, School of Neurology, Neurobiology and Psychiatry, Faculty of Medical Sciences, University of Newcastle upon Tyne, NE2 4HH, UK E-mail: j.b.harris{at}ncl.ac.uk

ß-Bungarotoxin, a neurotoxic phospholipase A2 is a major fraction of the venom of kraits. The toxin was inoculated into one hind limb of young adult rats. The inoculated hind limb was paralysed within 3 h, and remained paralysed for 2 days. The paralysis was associated with the loss of synaptic vesicles from motor nerve terminal boutons, a decline in immunoreactivity of synaptophysin, SNAP-25 and syntaxin, a loss of muscle mass and the upregulation of NaV1.5 mRNA and protein. Between 3 and 6 h after the inoculation of toxin, some nerve terminal boutons exhibited clear signs of degeneration. Others appeared to be in the process of withdrawing from the synaptic cleft and some boutons were fully enwrapped in terminal Schwann cell processes. By 12 h all muscle fibres were denervated. Re-innervation began at 3 days with the appearance of regenerating nerve terminals, a return of neuromuscular function in some muscles and a progressive increase in the immunoreactivity of synaptophysin, SNAP-25 and syntaxin. Full recovery occurred at 7 days. The data were compared with recently published clinical data on envenoming bites by kraits and by extrapolation we suggest that the acute, reversible denervation caused by ß-bungarotoxin is a credible explanation for the clinically important, profound treatment-resistant neuromuscular paralysis seen in human subjects bitten by these animals.

Key Words: neuropharmacology; neuropathy; neuropathology; neuromuscular junction; neurobiology; snake-bite; krait

Abbreviations: NMJ = neuromuscular junction; PBS = phosphate-buffered saline.

Received April 28, 2005. Revised August 1, 2005. Accepted August 30, 2005.


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