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

Neuroreport
Maria A CasulaP Anand

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.

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Citations

Jul 17, 2013·Pain Medicine : the Official Journal of the American Academy of Pain Medicine·Graham M PitcherJames L Henry
Nov 25, 2006·Seminars in Cell & Developmental Biology·Marc RogersEdward B Stevens
Apr 25, 2006·The Journal of Pain : Official Journal of the American Pain Society·Ron AmirGary R Strichartz
Feb 8, 2019·Nature Reviews. Drug Discovery·Heike WulffVladimir Yarov-Yarovoy

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