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The pharmacology of voltage-gated sodium channel activators.
Neuropharmacology. 2017 Dec; 127:87-108.N

Abstract

Toxins and venom components that target voltage-gated sodium (NaV) channels have evolved numerous times due to the importance of this class of ion channels in the normal physiological function of peripheral and central neurons as well as cardiac and skeletal muscle. NaV channel activators in particular have been isolated from the venom of spiders, wasps, snakes, scorpions, cone snails and sea anemone and are also produced by plants, bacteria and algae. These compounds have provided key insight into the molecular structure, function and pathophysiological roles of NaV channels and are important tools due to their at times exquisite subtype-selectivity. We review the pharmacology of NaV channel activators with particular emphasis on mammalian isoforms and discuss putative applications for these compounds. This article is part of the Special Issue entitled 'Venom-derived Peptides as Pharmacological Tools.'

Authors+Show Affiliations

Centre for Pain Research, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Qld 4072, Australia.Centre for Pain Research, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Qld 4072, Australia.Centre for Pain Research, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Qld 4072, Australia.Centre for Pain Research, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Qld 4072, Australia; School of Pharmacy, The University of Queensland, Woolloongabba, Qld 4102, Australia. Electronic address: i.vetter@uq.edu.au.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

28416444

Citation

Deuis, Jennifer R., et al. "The Pharmacology of Voltage-gated Sodium Channel Activators." Neuropharmacology, vol. 127, 2017, pp. 87-108.
Deuis JR, Mueller A, Israel MR, et al. The pharmacology of voltage-gated sodium channel activators. Neuropharmacology. 2017;127:87-108.
Deuis, J. R., Mueller, A., Israel, M. R., & Vetter, I. (2017). The pharmacology of voltage-gated sodium channel activators. Neuropharmacology, 127, 87-108. https://doi.org/10.1016/j.neuropharm.2017.04.014
Deuis JR, et al. The Pharmacology of Voltage-gated Sodium Channel Activators. Neuropharmacology. 2017;127:87-108. PubMed PMID: 28416444.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The pharmacology of voltage-gated sodium channel activators. AU - Deuis,Jennifer R, AU - Mueller,Alexander, AU - Israel,Mathilde R, AU - Vetter,Irina, Y1 - 2017/04/14/ PY - 2017/02/13/received PY - 2017/03/28/revised PY - 2017/04/10/accepted PY - 2017/4/19/pubmed PY - 2018/7/12/medline PY - 2017/4/19/entrez KW - Activator KW - Pharmacology KW - Toxin KW - Voltage sensor KW - Voltage-gated sodium channel SP - 87 EP - 108 JF - Neuropharmacology JO - Neuropharmacology VL - 127 N2 - Toxins and venom components that target voltage-gated sodium (NaV) channels have evolved numerous times due to the importance of this class of ion channels in the normal physiological function of peripheral and central neurons as well as cardiac and skeletal muscle. NaV channel activators in particular have been isolated from the venom of spiders, wasps, snakes, scorpions, cone snails and sea anemone and are also produced by plants, bacteria and algae. These compounds have provided key insight into the molecular structure, function and pathophysiological roles of NaV channels and are important tools due to their at times exquisite subtype-selectivity. We review the pharmacology of NaV channel activators with particular emphasis on mammalian isoforms and discuss putative applications for these compounds. This article is part of the Special Issue entitled 'Venom-derived Peptides as Pharmacological Tools.' SN - 1873-7064 UR - https://www.unboundmedicine.com/medline/citation/28416444/The_pharmacology_of_voltage_gated_sodium_channel_activators_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0028-3908(17)30155-7 DB - PRIME DP - Unbound Medicine ER -