Expression of the sodium channel β3 subunit in injured human sensory neurons
2004; Lippincott Williams & Wilkins; Volume: 15; Issue: 10 Linguagem: Inglês
10.1097/01.wnr.0000134927.02776.ae
ISSN1473-558X
AutoresMaria Anna Casula, P. Facer, Andrew J. Powell, Ian J. Kinghorn, Christopher Plumpton, Simon Tate, C. Bountra, Rolfe Birch, Praveen Anand,
Tópico(s)Neuropeptides and Animal Physiology
ResumoVoltage-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.
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