The voltage-gated sodium channel Na(v)1.9 is an effector of peripheral inflammatory pain hypersensitivity.

The voltage-gated sodium channel Na(v)1.9 is an effector of peripheral inflammatory pain hypersensitivity. Research Abstract Details 

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The voltage-gated sodium channel Na(v)1.9 is an effector of peripheral inflammatory pain hypersensitivity. Abstract Text:

Fumimasa Amaya,Haibin Wang,Michael Costigan,Andrew J Allchorne,Jon P Hatcher,Julie Egerton,Tania Stean,Valerie Morisset,David Grose,Martin J Gunthorpe,Iain P Chessell,Simon Tate,Paula J Green,Clifford J Woolf,

We used a mouse with deletion of exons 4, 5, and 6 of the SCN11A (sodium channel, voltage-gated, type XI, alpha) gene that encodes the voltage-gated sodium channel Na(v)1.9 to assess its contribution to pain. Na(v)1.9 is present in nociceptor sensory neurons that express TRPV1, bradykinin B2, and purinergic P2X3 receptors. In Na(v)1.9-/- mice, the non-inactivating persistent tetrodotoxin-resistant sodium TTXr-Per current is absent, whereas TTXr-Slow is unchanged. TTXs currents are unaffected by the mutation of Na(v)1.9. Pain hypersensitivity elicited by intraplantar administration of prostaglandin E2, bradykinin, interleukin-1beta, capsaicin, and P2X3 and P2Y receptor agonists, but not NGF, is either reduced or absent in Na(v)1.9-/- mice, whereas basal thermal and mechanical pain sensitivity is unchanged. Thermal, but not mechanical, hypersensitivity produced by peripheral inflammation (intraplanatar complete Freund's adjuvant) is substantially diminished in the null allele mutant mice, whereas hypersensitivity in two neuropathic pain models is unchanged in the Na(v)1.9-/- mice. Na(v)1.9 is, we conclude, an effector of the hypersensitivity produced by multiple inflammatory mediators on nociceptor peripheral terminals and therefore plays a key role in mediating peripheral sensitization.

The voltage-gated sodium channel Na(v)1.9 is an effector of peripheral inflammatory pain hypersensitivity. Publishing Authors By Initials

F Amaya,H Wang,M Costigan,AJ Allchorne,JP Hatcher,J Egerton,T Stean,V Morisset,D Grose,MJ Gunthorpe,IP Chessell,S Tate,PJ Green,CJ Woolf,

For similar proteins: carrier proteins: membrane transport proteins: ion channels: sodium channels research abstracts see: proteins: carrier proteins: membrane transport proteins: ion channels: sodium channels research

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The voltage-gated sodium channel Na(v)1.9 is an effector of peripheral inflammatory pain hypersensitivity. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of neuroscience : the official journal

VOLUME: 26

Page Numbers: 12852-60

Journal Abbreviation: J. Neurosci.

ISSN: 1529-2401

DAY: 13

MONTH: Dec

YEAR: 2006

The voltage-gated sodium channel Na(v)1.9 is an effector of peripheral inflammatory pain hypersensitivity. Information

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LANGUAGE: eng

NlmUniqueID: 8102140

The voltage-gated sodium channel Na(v)1.9 is an effector of peripheral inflammatory pain hypersensitivity. Keywords Mesh Terms:

KEYWORDS: Sodium Channels

MESH TERMS: genetics

Chemical & Substance for Abstract: The voltage-gated sodium channel Na(v)1.9 is an effector of peripheral inflammatory pain hypersensitivity. Information

Substance Name: Sodium Channels

Registry Number: 0

Grant and Affiliation Information for The voltage-gated sodium channel Na(v)1.9 is an effector of peripheral inflammatory pain hypersensitivity.

AFFILIATION: Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA.

Country: United States

AGENCY: United States NINDS

GRANT: NS38253

ACRONYM: NS

MEDLINETA: J Neurosci

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