Referenced in: none

Automatically associated channels: Nav1.3 , Nav1.8

Title: Expression of the sodium channel beta3 subunit in injured human sensory neurons.

Authors: Maria A Casula, Paul Facer, Andrew J Powell, Ian J Kinghorn, Christopher Plumpton, Simon N Tate, Chas Bountra, Rolfe Birch, Praveen Anand

Journal, date & volume: Neuroreport, 2004 Jul 19 , 15, 1629-32

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/15232296

Abstract
Voltage-gated sodium channel alpha-subunits play a key role in pain pathophysiology, and are modulated by beta-subunits. We previously reported that beta1- and beta2-subunits were decreased in human sensory neurons after spinal root avulsion injury. We have now detected, by immunohistochemistry, beta3-subunits in 82% of small/medium and 67% of large diameter sensory neurons in intact human dorsal root ganglia: 54% of beta3 small/medium neurons were NGF receptor trkA negative. Unlike beta1- and beta2, beta3-immunoreactivity did not decrease after avulsion injury, and the beta3:neurofilament ratio was significantly increased in proximal injured human nerves. beta3-subunit expression may thus be regulated differently from beta1, beta2 and Nav1.8. Targeting beta3 interactions with key alpha-subunits, particularly Nav1.3 and Nav1.8, may provide novel selective analgesics.