Abstract
Venoms often target vital processes to cause paralysis or death, but many types of venom also elicit notoriously intense pain. While these pain-producing effects can result as a byproduct of generalized tissue trauma, there are now multiple examples of venom-derived toxins that target somatosensory nerve terminals in order to activate nociceptive (pain-sensing) neural pathways. Intriguingly, investigation of the venom components that are responsible for evoking pain has revealed novel roles and/or configurations of well-studied toxin motifs. This review serves to highlight pain-producing toxins that target the capsaicin receptor, TRPV1, or members of the acid-sensing ion channel family, and to discuss the utility of venom-derived multivalent and multimeric complexes.
Copyright © 2012 Elsevier Ltd. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Acid Sensing Ion Channels
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Acute Pain / chemically induced*
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Acute Pain / etiology
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Acute Pain / metabolism
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Animals
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Bites and Stings / metabolism
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Bites and Stings / physiopathology
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Ganglia, Sensory / drug effects
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Ganglia, Sensory / metabolism
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Humans
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Nerve Tissue Proteins / agonists*
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Nerve Tissue Proteins / chemistry
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Nerve Tissue Proteins / metabolism
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Nociceptors / drug effects*
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Nociceptors / metabolism
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Protein Conformation
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Protein Subunits / analysis
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Protein Subunits / chemistry
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Protein Subunits / toxicity
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Proteins / analysis
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Proteins / chemistry
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Proteins / toxicity*
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Sodium Channel Agonists*
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Sodium Channels / chemistry
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Sodium Channels / metabolism
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Somatosensory Cortex / drug effects
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Somatosensory Cortex / metabolism
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TRPV Cation Channels / agonists*
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TRPV Cation Channels / chemistry
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TRPV Cation Channels / metabolism
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Venoms / chemistry
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Venoms / enzymology
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Venoms / toxicity*
Substances
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Acid Sensing Ion Channels
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Nerve Tissue Proteins
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Protein Subunits
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Proteins
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Sodium Channel Agonists
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Sodium Channels
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TRPV Cation Channels
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TRPV1 receptor
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Venoms