The gene SCN10A (also known as PN3; SNS; hPN3; Nav1.8) encodes the voltage-gated sodium channel alpha subunit, type X, Na1.8. SCN10A encodes a TTX-resistant channel that is restricted to the peripheral sensory nervous system .
Nav1.8 is found only within small-diameter sensory neurons in the periphery generating electrical impulses and transmiting nociceptive information to the central nervous system in cold temperatures, unlike the other sodium channels which have enhanced slow inactivation with cooling .
Scn10a : sodium channel, voltage-gated, type X, alpha subunit
Nav1.8 channels interact with various commercially available compounds such as menthol, lidocaine, tetracaine, vinpocetine, ambroxol, lamotrigine, mexilitine, veratridine, and A-803467, whereas very few animal toxins have been shown to be capable of reshaping Nav1.8 currents . For example, lidocaine,
suppresses Na+ currents by binding not only to DIV–S6 but also to S6 of DI and DII, blocking the channels in a use-dependent (frequency-dependent) and voltage-dependent manner , . Lidocaine enhanced current decrease in a frequency-dependent manner. Steady-state inactivation of Nav1.8 and Nav1.7 channels was also affected by lidocaine, Nav1.7 being the most sensitive. Only the steady-state activation of Nav1.8 was affected while the entry of both channels into slow inactivation was affected by lidocaine, Nav1.8 being affected to a larger degree. 
Nav1.8 is likely to be co-expressed with the b1, b2, and b3-subunits in C-fiber neurons from the DRG, and these subunits interact and modulate the channel.
b1-subunit alone, or in combination with other b-subunits, accelerates the time constant of inactivation and shifts the voltage-dependence of activation to more hyperpolarized potentials. Beta-1 also increases levels of Nav1.8 channel functional expression, either by increasing channel density at the oocyte membrane or by increasing individual channel conductance.
b3-subunit shifts the voltage-dependence of inactivation to more positive potentials and do not influence the time constant of current decay, steadystate activation or expression of Nav1.8. Co-expression of b1 and b3-subunits with Nav1.8 resulted in little change in availability compared to channel alone.
b2-subunit do not alter the kinetic properties or current amplitude of However, the co-expression of b1 and b2 shift the Nav1.8 channel availability to more depolarized potentials in comparison to when channels are expressed with either b1 or b2 alone.
The a-subunit - such as Nav1.8 - is composed of
four homologous domains (DI–DIV), each of which is
composed of six transmembrane segments (S1–S6).
Nav1.8 is expressed both in the soma of IB4+ and IB4- cells  and in the axons  of the dorsal root glanlia. It has been also expressed in the somas located of the rat trigemina ganglia .
The channel is expressed only by small-diameter sensory neurons in neonatal and adult dorsal root and trigeminal ganglia .
Nociceptive dorsal root ganglion (DRG) neurons can be classified into nonpeptidergic IB4+ and peptidergic IB4- subtypes, which terminate in different layers in dorsal horn and transmit pain along different ascending pathways, and display different firing properties. Voltage-gated, tetrodotoxin-resistant (TTX-R)
Nav1.8 channels are expressed in both IB4+ and IB4- cells and produce most of the current underlying the depolarizing phase of action potential (AP). use-dependent reduction of Nav1.8 current in IB4+ neurons is significantly stronger than that in IB4- neurons, although voltage dependency of activation and steady-state inactivation are not different.
Nav1.8 is detected in unmyelinated fibers innervating cornea  and it has been reported at 20% of nodes of Ranvier in myelinated axons that innervate tooth pulp .
The Nav1.8 channel is able to reactivate rapidly and can still sending action potentials to the central nervous systemeven when other channels remain desensitized .
Gain-of-function changes caused by mutations increase the excitability of DRG neurons. These observations suggest that Nav1.8 mutations contribute to pain in some peripheral neuropathies :
* Visceral pain 
* Cold pain 
* Mechanical and inflammatory pain 
Nav1.8, together with Nav1.7, accumulates in painful human neuromas and is responsible for ectopic axonal hyper excitability, resulting in abnormal sensory phenomena such as pain and paresthesias .
Nav1.8 produces a slowly inactivating sodium current
characterized by depolarized voltage dependency ,  and rapid recovery from
fast inactivation , , . Nav1.8 channels produce the majority of the inward current during the AP upstroke
in the DRG neurons in which they are present , , most of which are nociceptive
. TTX-R currents attributable to Nav1.8
enter rapidly into, and recover slowly from, slow inactivation
even during short depolarizing pulses from holding potentials
near resting membrane potential, thereby contributing to adaptation of firing in response to capsaicin application . (This summary is from )