title: Animal toxins can alter the function of Nav1.8 and Nav1.9.
abstract: 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.
authors.affiliation: Department of Physiology, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA.
authors.forename: John
authors.initials: J
authors.lastname: Gilchrist
authors.forename: Frank
authors.initials: F
authors.lastname: Bosmans
mesh_terms: D000818:Animals; D006801:Humans; D062559:NAV1.8 Voltage-Gated Sodium Channel / Q000502:physiology*; D062558:NAV1.9 Voltage-Gated Sodium Channel / Q000502:physiology*; D010146:Pain / Q000503:physiopathology; D058748:Pain Perception / Q000502:physiology*; D014118:Toxins, Biological / Q000494:pharmacology*
chemical_list: D062559:NAV1.8 Voltage-Gated Sodium Channel; D062558:NAV1.9 Voltage-Gated Sodium Channel; D014118:Toxins, Biological