Expression of the sodium channel β3 subunit in injured human sensory neurons

被引：21

作者：

Casula, MA

Facer, P

Powell, AJ

Kinghorn, IJ

Plumpton, C

Tate, SN

Bountra, C

Birch, R

Arland, P

机构：

[1] Hammersmith Hosp, Imperial Coll London, Peripheral Neuropathy Unit, London W12 0NN, England

[2] GlaxoSmithKline, Gene Express & Prot Biochem, Stevenage SG1 2NY, Herts, England

[3] GlaxoSmithKline, Neurol & GI CEDD, Harlow CM19 5AW, Essex, England

[4] Royal Natl Orthopaed Hosp, Peripheral Nerve Injury Unit, Stanmore HA7 4LP, Middx, England

来源：

NEUROREPORT | 2004年 / 15卷 / 10期

关键词：

beta-subunit; DRG; human; nociceptors; sensory neurons; sodium channel; trkA;

D O I：

10.1097/01.wnr.0000134927.02776.ae

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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 Na(v)1.8. Targeting beta3 interactions with key alpha-subunits, particularly Na(v)1.3 and Na(v)1.8, may provide novel selective analgesics.

引用

页码：1629 / 1632

页数：4

共 26 条

[21] β3, a novel auxiliary subunit for the voltage-gated sodium channel, is expressed preferentially in sensory neurons and is upregulated in the chronic constriction injury model of neuropathic pain [J].