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Voltage‐gated sodium channels: (Na V )igating the field to determine their contribution to visceral nociception
Author(s) -
Erickson Andelain,
Deiteren Annemie,
Harrington Andrea M.,
GarciaCaraballo Sonia,
Castro Joel,
Caldwell Ashlee,
Grundy Luke,
Brierley Stuart M.
Publication year - 2018
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jp273461
Subject(s) - sodium channel , visceral pain , nociception , gastrointestinal tract , motility , medicine , abdominal pain , endocrinology , sodium , neuroscience , chemistry , biology , receptor , microbiology and biotechnology , organic chemistry
Chronic visceral pain, altered motility and bladder dysfunction are common, yet poorly managed symptoms of functional and inflammatory disorders of the gastrointestinal and urinary tracts. Recently, numerous human channelopathies of the voltage‐gated sodium (Na V ) channel family have been identified, which induce either painful neuropathies, an insensitivity to pain, or alterations in smooth muscle function. The identification of these disorders, in addition to the recent utilisation of genetically modified Na V mice and specific Na V channel modulators, has shed new light on how Na V channels contribute to the function of neuronal and non‐neuronal tissues within the gastrointestinal tract and bladder. Here we review the current pre‐clinical and clinical evidence to reveal how the nine Na V channel family members (Na V 1.1–Na V 1.9) contribute to abdominal visceral function in normal and disease states.