Literature DB >> 24365366

Venomous snake bites, scorpions, and spiders.

S A M Kularatne1, Nimal Senanayake2.   

Abstract

Neurologic dysfunction due to natural neurotoxins is an important, but neglected, public health hazard in many parts of the world, particularly in the tropics. These toxins are produced by or found among a variety of live forms that include venomous snakes, arthropods such as scorpions, spiders, centipedes, stinging insects (Hymenoptera), ticks, certain poisonous fish, shellfish, crabs, cone shells, skin secretions of dart-poison frogs, and bacterial poisons such as botulinum toxin. These toxins commonly act on neuromuscular transmission at the neuromuscular junction where acetylcholine is the neurotransmitter, but in certain situations the toxins interfere with neurotransmitters such as GABA, noradrenaline, adrenaline, dopamine, and γ-aminobutyrate. Of the toxins, α-toxins and κ-toxins (e.g., Chinese krait, Bungarus multicinctus) act on the postsynaptic membrane, blocking the receptors, whilst β-toxin (e.g., common krait, B. caeruleus) acts on the presynaptic membrane, causing impairment of acetylcholine release. Conversely, dendrotoxins of the African mamba enhance acetylcholine release. The toxins of scorpions and spiders commonly interfere with voltage-gated ion channels. Clinically, the cardinal manifestation is muscle paralysis. In severe cases respiratory paralysis could be fatal. Effective antivenoms are the mainstay of treatment of envenoming, but their lack of availability is the major concern in the regions of the globe where they are desperately needed. Interestingly, some toxins have proved to be valuable pharmaceutical agents, while some others are widely exploited to study neuromuscular physiology and pathology.
© 2014 Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Hymenoptera; Snakes; envenoming; neuromuscular junction; neurotoxins; paralysis; poisonous fish; scorpions; spiders

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Substances:

Year:  2014        PMID: 24365366     DOI: 10.1016/B978-0-7020-4087-0.00066-8

Source DB:  PubMed          Journal:  Handb Clin Neurol        ISSN: 0072-9752


  7 in total

1.  Mitochondrial alarmins released by degenerating motor axon terminals activate perisynaptic Schwann cells.

Authors:  Elisa Duregotti; Samuele Negro; Michele Scorzeto; Irene Zornetta; Bryan C Dickinson; Christopher J Chang; Cesare Montecucco; Michela Rigoni
Journal:  Proc Natl Acad Sci U S A       Date:  2015-01-20       Impact factor: 11.205

Review 2.  Centipede Venom: A Potential Source of Ion Channel Modulators.

Authors:  Anna Luo; Aili Wang; Peter Muiruri Kamau; Ren Lai; Lei Luo
Journal:  Int J Mol Sci       Date:  2022-06-26       Impact factor: 6.208

Review 3.  Why do we study animal toxins?

Authors:  Yun Zhang
Journal:  Dongwuxue Yanjiu       Date:  2015-07-18

4.  ATP Released by Injured Neurons Activates Schwann Cells.

Authors:  Samuele Negro; Elisanna Bergamin; Umberto Rodella; Elisa Duregotti; Michele Scorzeto; Kees Jalink; Cesare Montecucco; Michela Rigoni
Journal:  Front Cell Neurosci       Date:  2016-05-23       Impact factor: 5.505

Review 5.  Bioactive Peptides and Proteins from Centipede Venoms.

Authors:  Yalan Han; Peter Muiruri Kamau; Ren Lai; Lei Luo
Journal:  Molecules       Date:  2022-07-11       Impact factor: 4.927

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

Authors:  Elisa Duregotti; Giulia Zanetti; Michele Scorzeto; Aram Megighian; Cesare Montecucco; Marco Pirazzini; Michela Rigoni
Journal:  Toxins (Basel)       Date:  2015-12-08       Impact factor: 4.546

7.  Jingzhaotoxin-X, a gating modifier of Kv4.2 and Kv4.3 potassium channels purified from the venom of the Chinese tarantula Chilobrachys jingzhao.

Authors:  Meichun Deng; Liping Jiang; Xuan Luo; Huai Tao; Songping Liang
Journal:  J Venom Anim Toxins Incl Trop Dis       Date:  2020-05-29
  7 in total

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