From genes to pain: Nav1.7 and human pain disorders

Sulayman D. Dib-Hajj, Theodore Cummins, Joel A. Black, Stephen G. Waxman

Research output: Contribution to journalArticle

188 Citations (Scopus)

Abstract

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 Nav1.7 is expressed preferentially in most slowly conducting nociceptive neurons and in sympathetic neurons. Gain-of-function mutations in the Nav1.7 channel lead to DRG neuron hyperexcitability associated with severe pain, whereas loss of the Nav1.7 channel in patients leads to indifference to pain. The contribution of Nav1.7 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.

Original languageEnglish
Pages (from-to)555-563
Number of pages9
JournalTrends in Neurosciences
Volume30
Issue number11
DOIs
StatePublished - Nov 2007

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Somatoform Disorders
Pain
Genes
Voltage-Gated Sodium Channels
Neurons
Nociceptors
Mutation
Sodium Channels
Diagnosis-Related Groups
Acute Pain
Neuralgia
Chronic Pain
Therapeutics

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

From genes to pain : Nav1.7 and human pain disorders. / Dib-Hajj, Sulayman D.; Cummins, Theodore; Black, Joel A.; Waxman, Stephen G.

In: Trends in Neurosciences, Vol. 30, No. 11, 11.2007, p. 555-563.

Research output: Contribution to journalArticle

Dib-Hajj, Sulayman D. ; Cummins, Theodore ; Black, Joel A. ; Waxman, Stephen G. / From genes to pain : Nav1.7 and human pain disorders. In: Trends in Neurosciences. 2007 ; Vol. 30, No. 11. pp. 555-563.
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