From genes to pain: Na v 1.7 and human pain disorders

Trends Neurosci. 2007 Nov;30(11):555-63. doi: 10.1016/j.tins.2007.08.004. Epub 2007 Oct 22.


Gain-of-function mutations or dysregulated expression of voltage-gated sodium channels can produce neuronal hyperexcitability, leading to acute or chronic pain. The sodium channel Na(v)1.7 is expressed preferentially in most slowly conducting nociceptive neurons and in sympathetic neurons. Gain-of-function mutations in the Na(v)1.7 channel lead to DRG neuron hyperexcitability associated with severe pain, whereas loss of the Na(v)1.7 channel in patients leads to indifference to pain. The contribution of Na(v)1.7 to acquired and inherited pain states and the absence of motor, cognitive and cardiac deficits in patients lacking this channel make it an attractive target for the treatment of neuropathic pain.

Publication types

  • Review

MeSH terms

  • Animals
  • Ganglia, Spinal / cytology
  • Humans
  • Models, Animal
  • Mutation*
  • NAV1.7 Voltage-Gated Sodium Channel
  • Neurons / physiology
  • Sodium Channels / genetics*
  • Somatoform Disorders / genetics*
  • Somatoform Disorders / physiopathology*


  • NAV1.7 Voltage-Gated Sodium Channel
  • SCN9A protein, human
  • Sodium Channels