The pharmacology of voltage-gated sodium channel activators

被引:57
作者
Deuis, Jennifer R. [1 ]
Mueller, Alexander [1 ]
Israel, Mathilde R. [1 ]
Vetter, Irina [1 ,2 ]
机构
[1] Univ Queensland, Inst Mol Biosci, Ctr Pain Res, St Lucia, Qld 4072, Australia
[2] Univ Queensland, Sch Pharm, Woolloongabba, Qld 4102, Australia
基金
澳大利亚研究理事会;
关键词
Voltage-gated sodium channel; Activator; Toxin; Voltage sensor; Pharmacology; SEA-ANEMONE TOXINS; ALPHA-SCORPION TOXIN; SEVERE MYOCLONIC EPILEPSY; COMMON RECEPTOR-SITE; SPIDER DELTA-TOXIN; NA+ CHANNELS; RAT-BRAIN; FAST INACTIVATION; SKELETAL-MUSCLE; BETA-SUBUNITS;
D O I
10.1016/j.neuropharm.2017.04.014
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Toxins and venom components that target voltage-gated sodium (Nay) 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. Nay 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 Nay channels and are important tools due to their at times exquisite subtype-selectivity. We review the pharmacology of Nay 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.' (C) 2017 Elsevier Ltd. All rights reserved.
引用
收藏
页码:87 / 108
页数:22
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