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

Journal article

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.

Authors: Casula, M; Facer, P; Powell, A; Kinghorn, I; Plumpton, C

• Publication status: Published
• Journal: Neuroreport
• Volume: 15
• Issue: 10
• Pages: 1629-1632
• Publication date: 2004-07-01
• DOI: 10.1097/01.wnr.0000134927.02776.ae
• EISSN: 1473-558X
• ISSN: 0959-4965
• Language: English
• Keywords: Humans; Time Factors; Blotting, Western; Adult; Cell Line; Neurons, Afferent; Neurofilament Proteins; Aged; Gene Expression Regulation; Protein Subunits; Immunohistochemistry; Transfection; Embryo, Mammalian; Ganglia, Spinal; Sodium Channels