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Toxins 2013, 5(2), 286-314; doi:10.3390/toxins5020286

Venom Peptides as a Rich Source of Cav2.2 Channel Blockers

Institute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland, 4072, Australia
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Received: 2 November 2012 / Revised: 7 January 2013 / Accepted: 25 January 2013 / Published: 4 February 2013
(This article belongs to the Special Issue Animal Toxins Targeting Ion Channels Involved in Pain)
View Full-Text   |   Download PDF [1170 KB, 6 February 2013; original version 4 February 2013]   |  

Abstract

Cav2.2 is a calcium channel subtype localized at nerve terminals, including nociceptive fibers, where it initiates neurotransmitter release. Cav2.2 is an important contributor to synaptic transmission in ascending pain pathways, and is up-regulated in the spinal cord in chronic pain states along with the auxiliary α2δ1 subunit. It is therefore not surprising that toxins that inhibit Cav2.2 are analgesic. Venomous animals, such as cone snails, spiders, snakes, assassin bugs, centipedes and scorpions are rich sources of remarkably potent and selective Cav2.2 inhibitors. However, side effects in humans currently limit their clinical use. Here we review Cav2.2 inhibitors from venoms and their potential as drug leads.
Keywords: Cav2.2; voltage-gated calcium channels; nociception; neurotransmitter; ω-conotoxins; venom peptides Cav2.2; voltage-gated calcium channels; nociception; neurotransmitter; ω-conotoxins; venom peptides
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This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Sousa, S.R.; Vetter, I.; Lewis, R.J. Venom Peptides as a Rich Source of Cav2.2 Channel Blockers. Toxins 2013, 5, 286-314.

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