Selective voltage-gated sodium channel peptide toxins from animal venom: pharmacological probes and analgesic drug development.

Voltage-gated sodium channels (Navs) play critical roles in action potential generation and propagation. Nav channelopathy as well as pathological sensitization contribute to allodynia and hyperalgesia. Recent evidence has demonstrated the significant roles of Nav subtypes (Nav1.3, 1.7, 1.8 and 1.9) in nociceptive transduction and therefore these Navs may represent attractive targets for analgesic drug discovery. Animal toxins are structurally diverse peptides that are highly potent yet selective on ion channel subtypes and therefore representing valuable probes to elucidate the structures, gating properties and cellular functions of ion channels. In this review, we summarized recent advance of peptide toxins from animal venom that selectively target Nav1.3, 1.7, 1.8, and 1.9, along with their potentials in analgesic drug discovery.