Abstract
Pain is a common symptom induced during envenomation by spiders and scorpions. Toxins isolated from their venom have become essential tools for studying the functioning and physiopathological role of ion channels, as they modulate their activity. In particular, toxins that induce pain relief effects can serve as a molecular basis for the development of future analgesics in humans. This review provides a summary of the different scorpion and spider toxins that directly interact with pain-related ion channels, with inhibitory or stimulatory effects. Some of these toxins were shown to affect pain modalities in different animal models providing information on the role played by these channels in the pain process. The close interaction of certain gating-modifier toxins with membrane phospholipids close to ion channels is examined along with molecular approaches to improve selectivity, affinity or bioavailability in vivo for therapeutic purposes.
Highlights
Scorpions and spiders are venomous animals belonging to the arachnid class of arthropods
Scorpion venom peptides mainly consist of neuropeptides, cardiopeptides and antimicrobial peptides with cytotoxic activities [1], whereas spider venom is composed of more neuroactive peptides, a few cardiotoxic and antimicrobial peptides, and enzymatic proteins contributing to paralysis, death and tissue digestion during prey feeding [2,3,4]
BmK AGAP (Antitumor AnalGesic Peptide) another α-toxin isolated from Buthus martensii, has analgesic properties in a mice visceral model induced by ip acetic acid injections, and in inflammatory pain induced by peripheral injection of formalin [146]
Summary
Scorpions and spiders are venomous animals belonging to the arachnid class of arthropods. The β-toxin Cn2 isolated from Centruroides noxius venom is a specific activator of Nav1.6 channels, which play an essential role in pain transmission in peripheral sensory neurons. BmK AGAP (Antitumor AnalGesic Peptide) another α-toxin isolated from Buthus martensii, has analgesic properties in a mice visceral model induced by ip acetic acid injections, and in inflammatory pain induced by peripheral injection of formalin [146].
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