Nav1.8 is a voltage-gated sodium channel alpha subunit. It is expressed in mammalian adult dorsal root ganglion (DRG) neurons, predominantly those with small diameter cell bodies that give rise to the unmyelinated (C-type) fibres. These fibres form synapses in the dorsal horn of the spinal cord and are mainly involved in pain signaling. This channel conducts the characteristic slow, tetrodotoxin-resistant (TTX-r) currents involved in action potential initiation and transmission in these neurons and is therefore a potential target for analgesic agents. Altered expression of Nav1.8 is observed in pain models and human pain states-channel protein can be seen to re-localise from cell bodies to the site of insult or injury. There is also good evidence from antisense oligonucleotide studies for a role in development of hyperexciteable states in pain models. However KO mice show surprisingly limited pain phenotypes, possibly due to compensatory up-regulation of other Nav subtypes. Native sodium channels are multi-subunit complexes, composed of not only the pore forming alpha subunit, but also auxiliary beta subunits. The beta1 subunit is known to increase peak current amplitude as well as increasing sodium ion channel expression at the cell surface.