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Toxins 2015, 7(12), 5322-5336; doi:10.3390/toxins7124887

Snake and Spider Toxins Induce a Rapid Recovery of Function of Botulinum Neurotoxin Paralysed Neuromuscular Junction

1
Department of Biomedical Sciences, University of Padua, Via U. Bassi 58/B, 35131 Padova, Italy
2
Institute for Neuroscience, National Research Council, Via U. Bassi 58/B, 35131 Padova, Italy
*
Authors to whom correspondence should be addressed.
Academic Editor: Wolfgang Wüster
Received: 23 October 2015 / Revised: 20 November 2015 / Accepted: 30 November 2015 / Published: 8 December 2015
(This article belongs to the Section Animal Venoms)
View Full-Text   |   Download PDF [3838 KB, uploaded 8 December 2015]   |  

Abstract

Botulinum neurotoxins (BoNTs) and some animal neurotoxins (β-Bungarotoxin, β-Btx, from elapid snakes and α-Latrotoxin, α-Ltx, from black widow spiders) are pre-synaptic neurotoxins that paralyse motor axon terminals with similar clinical outcomes in patients. However, their mechanism of action is different, leading to a largely-different duration of neuromuscular junction (NMJ) blockade. BoNTs induce a long-lasting paralysis without nerve terminal degeneration acting via proteolytic cleavage of SNARE proteins, whereas animal neurotoxins cause an acute and complete degeneration of motor axon terminals, followed by a rapid recovery. In this study, the injection of animal neurotoxins in mice muscles previously paralyzed by BoNT/A or /B accelerates the recovery of neurotransmission, as assessed by electrophysiology and morphological analysis. This result provides a proof of principle that, by causing the complete degeneration, reabsorption, and regeneration of a paralysed nerve terminal, one could favour the recovery of function of a biochemically- or genetically-altered motor axon terminal. These observations might be relevant to dying-back neuropathies, where pathological changes first occur at the neuromuscular junction and then progress proximally toward the cell body. View Full-Text
Keywords: botulinum neurotoxins; animal neurotoxins; nerve terminals degeneration; mouse; DAS assay; paralysis; neuroexocytosis botulinum neurotoxins; animal neurotoxins; nerve terminals degeneration; mouse; DAS assay; paralysis; neuroexocytosis
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Duregotti, E.; Zanetti, G.; Scorzeto, M.; Megighian, A.; Montecucco, C.; Pirazzini, M.; Rigoni, M. Snake and Spider Toxins Induce a Rapid Recovery of Function of Botulinum Neurotoxin Paralysed Neuromuscular Junction. Toxins 2015, 7, 5322-5336.

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