SOMATOSENSORY SYSTEMS, PAINExpression of the sodium channel β3 subunit in injured human sensory neuronsCasula, Maria A.; Facer, Paul; Powell, Andrew J.1; Kinghorn, Ian J.1; Plumpton, Christopher1; Tate, Simon N.1; Bountra, Chas2; Birch, Rolfe3; Anand, PraveenCACAAuthor Information Peripheral Neuropathy Unit, Imperial College London, Area A, Ground Floor, Hammersmith Hospital, Du Cane Rd, London W12 0NN 1Gene Expression and Protein Biochemistry, GlaxoSmithKline, Stevenage, Hertfordshire, SG1 2NY 2Neurology and GI CEDD, GlaxoSmithKline, New Frontiers Science Park, Harlow, Essex, CM19 5AW 3Peripheral Nerve Injury Unit, Royal National Orthopaedic Hospital, Stanmore, Middlesex HA7 4LP, UK CACorresponding Author: firstname.lastname@example.org Received 5 March 2004; accepted 17 March 2004 NeuroReport: July 19th, 2004 - Volume 15 - Issue 10 - p 1629-1632 doi: 10.1097/01.wnr.0000134927.02776.ae Buy SDC Metrics Abstract Voltage-gated sodium channel α-subunits play a key role in pain pathophysiology, and are modulated by β-subunits. We previously reported that β1- and β2-subunits were decreased in human sensory neurons after spinal root avulsion injury. We have now detected, by immunohistochemistry, β3-subunits in 82% of small/medium and 67% of large diameter sensory neurons in intact human dorsal root ganglia: 54% of β3 small/medium neurons were NGF receptor trkA negative. Unlike β1- and β2, β3-immunoreactivity did not decrease after avulsion injury, and the β3:neurofilament ratio was significantly increased in proximal injured human nerves. β3-subunit expression may thus be regulated differently from β1, β2 and Nav1.8. Targeting β3 interactions with key α-subunits, particularly Nav1.3 and Nav1.8, may provide novel selective analgesics. © 2004 Lippincott Williams & Wilkins, Inc.