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The voltage‐gated sodium channel Na V 1.9 in visceral pain
Author(s) -
Hockley J. R. F.,
Winchester W. J.,
Bulmer D. C.
Publication year - 2016
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/nmo.12698
Subject(s) - visceral pain , pathophysiology , sodium channel , medicine , disease , bioinformatics , gastroenterology , sodium , nociception , receptor , biology , chemistry , organic chemistry
Background Visceral pain is a common symptom for patients with gastrointestinal ( GI ) disease. It is unpleasant, debilitating, and represents a large unmet medical need for effective clinical treatments. Recent studies have identified Na V 1.9 as an important regulator of afferent sensitivity in visceral pain pathways to mechanical and inflammatory stimuli, suggesting that Na V 1.9 could represent an important therapeutic target for the treatment of visceral pain. This potential has been highlighted by the identification of patients who have an insensitivity to pain or painful neuropathies associated with mutations in SCN 11A , the gene encoding voltage‐gated sodium channel subtype 1.9 (Na V 1.9). Purpose Here, we address the role of Na V 1.9 in visceral pain and what known human Na V 1.9 mutants can tell us about Na V 1.9 function in gut physiology and pathophysiology.