Animal Toxins Can Alter the Function of Nav1.8 and Nav1.9

Toxins

John Gilchrist¹ 

[1] Department of Physiology, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA;

关键词: Nav1.8;    Nav1.9;    pain;    animal toxins;    voltage sensor;    voltage-activated sodium channel;   

DOI  :  10.3390/toxins4080620

来源: mdpi

【 摘 要 】

Human voltage-activated sodium (Nav) channels are adept at rapidly transmitting electrical signals across long distances in various excitable tissues. As such, they are amongst the most widely targeted ion channels by drugs and animal toxins. Of the nine isoforms, Nav1.8 and Nav1.9 are preferentially expressed in DRG neurons where they are thought to play an important role in pain signaling. Although the functional properties of Nav1.8 have been relatively well characterized, difficulties with expressing Nav1.9 in established heterologous systems limit our understanding of the gating properties and toxin pharmacology of this particular isoform. This review summarizes our current knowledge of the role of Nav1.8 and Nav1.9 in pain perception and elaborates on the approaches used to identify molecules capable of influencing their function.

【 授权许可】

CC BY   
© 2012 by the authors; licensee MDPI, Basel, Switzerland.