Sodium channel β1 and β2 subunits parallel SNS/PN3 α-subunit changes in injured human sensory neurons

被引：36

作者：

Coward, K

Jowett, A

Plumpton, C

Powell, A

Birch, R

Tate, S

Bountra, C

Anand, P

机构：

[1] Imeprial Coll Sch Med, Peripheral Neuropathy Unit, London W12 0NN, England

[2] Glaxo Wellcome Res & Dev Ltd, Med Res Ctr, Mol Recognit Dept, Stevenage SG1 2NY, Herts, England

[3] Glaxo Wellcome Res & Dev Ltd, Med Res Ctr, Dept Mol Pharmacol, Stevenage SG1 2NY, Herts, England

[4] Glaxo Wellcome Res & Dev Ltd, Med Res Ctr, Neurol & Rheumatol, Stevenage SG1 2NY, Herts, England

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

来源：

NEUROREPORT | 2001年 / 12卷 / 03期

关键词：

beta subunit; human; SNS/PN3; sodium channel;

D O I：

10.1097/00001756-200103050-00012

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Voltage-gated sodium channels consist of a pore-containing alpha -subunit and one or more auxiliary beta -subunits. which may modulate channel function. We previously demonstrated that sodium channel SNS/PN3 alpha -subunits were decreased in human sensory cell bodies after spinal root avulsion injury. and accumulated at injured nerve terminals in pain states. Using specific antibodies for immunohistochemistry, we have now detected sodium channel beta1 and beta2 subunits in sensory cell bodies within control human postmortem sensory ganglia (78% of small/medium (less than or equal to 50 mum) and 68% of large (greater than or equal to 50 mum) cells); their changes in cervical sensory ganglia after avulsion injury paralleled those described for SNS/PN3 alpha -subunits. Our results suggest that alpha- and beta -subunits share common regulatory mechanisms, but present distinct targets for novel analgesics. NeuroReport 12:483-488 (C) 2001 Lippincott Williams & Wilkins.

引用

页码：483 / 488

页数：6

共 19 条

[1] The sodium channel auxiliary subunits β1 and β2 are differentially expressed in the spinal cord of neuropathic rats [J].