Sodium Channels in Normal and Pathological Pain

被引：483

作者：

Dib-Hajj, Sulayman D. ^{[1
,2
,3
]}

Cummins, Theodore R. ^{[4
]}

Black, Joel A. ^{[1
,2
,3
]}

Waxman, Stephen G. ^{[1
,2
,3
]}

机构：

[1] Yale Univ, Sch Med, Dept Neurol, New Haven, CT 06510 USA

[2] Yale Univ, Sch Med, Ctr Neurosci & Regenerat Res, New Haven, CT 06510 USA

[3] Vet Affairs Connecticut Healthcare Syst, Rehabil Res Ctr, West Haven, CT 06516 USA

[4] Indiana Univ, Sch Med, Dept Pharmacol & Toxicol, Stark Neurosci Inst, Indianapolis, IN 46202 USA

来源：

ANNUAL REVIEW OF NEUROSCIENCE, VOL 33 | 2010年 / 33卷

关键词：

erythromelalgia; paroxysmal extreme pain disorder; congenital insensitivity to pain; sensory neurons; sympathetic neurons; DORSAL-ROOT GANGLION; RESISTANT NA+ CURRENT; SPINAL SENSORY NEURONS; CLOSED-STATE INACTIVATION; NERVE GROWTH-FACTOR; OF-FUNCTION MUTATIONS; TETRODOTOXIN-RESISTANT; NEUROPATHIC PAIN; PROTEIN-KINASE; ELECTROPHYSIOLOGICAL PROPERTIES;

D O I：

10.1146/annurev-neuro-060909-153234

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Nociception is essential for survival whereas pathological pain is maladaptive and often unresponsive to pharmacotherapy. Voltage-gated sodium channels, Na-v 1.1-Na-v 1.9, are essential for generation and conduction of electrical impulses in excitable cells. Human and animal studies have identified several channels as pivotal for signal transmission along the pain axis, including Na-v 1.3, Na-v 1.7, Na-v 1.8, and Na-v 1.9, With the latter three preferentially expressed in peripheral sensory neurons and Na-v 1.3 being upregulated along pain-signaling pathways after nervous system injuries. Na-v 1.7 is of special interest because it has been linked to a spectrum of inherited human pain disorders. Here we review the contribution of these sodium channel isoforms to pain.

引用

页码：325 / 347

页数：23

共 167 条

[1] The cell and molecular basis of mechanical, cold, and inflammatory pain [J].

Abrahamsen, Bjarke ;

Zhao, Jing ;

Asante, Curtis O. ;

Cendan, Cruz Miguel ;

Marsh, Steve ;

Martinez-Barbera, Juan Pedro ;

Nassar, Mohammed A. ;

Dickenson, Anthony H. ;

Wood, John N. .

SCIENCE, 2008, 321 (5889) :702-705

[2] A stop codon mutation in SCN9A causes lack of pain sensation [J].

Ahmad, Sultan ;

Dahllund, Leif ;

Eriksson, Anders B. ;

Hellgren, Dennis ;

Karlsson, Urban ;

Lund, Per-Eric ;

Meijer, Inge A. ;

Meury, Luc ;

Mills, Tracy ;

Moody, Adrian ;

Morinville, Anne ;

Morten, John ;

O'Donnell, Dajan ;

Raynoschek, Carina ;

Salter, Hugh ;

Rouleau, Guy A. ;

Krupp, Johannes J. .

HUMAN MOLECULAR GENETICS, 2007, 16 (17) :2114-2121

[3] The tetrodotoxin-resistant sodium channel SNS has a specialized function in pain pathways [J].

Akopian, AN ;

Souslova, V ;

England, S ;

Okuse, K ;

Ogata, N ;

Ure, J ;

Smith, A ;

Kerr, BJ ;

McMahon, SB ;

Boyce, S ;

Hill, R ;

Stanfa, LC ;

Dickenson, AH ;

Wood, JN .

NATURE NEUROSCIENCE, 1999, 2 (06) :541-548

[4] A tetrodotoxin-resistant voltage-gated sodium channel expressed by sensory neurons [J].

Akopian, AN ;

Sivilotti, L ;

Wood, JN .

NATURE, 1996, 379 (6562) :257-262

[5] The voltage-gated sodium channel Nav1.9 is an effector of peripheral inflammatory pain hypersensitivity [J].

Amaya, Fumimasa ;

Wang, Haibin ;

Costigan, Michael ;

Allchorne, Andrew J. ;

Hatcher, Jon P. ;

Egerton, Julie ;

Stean, Tania ;

Morisset, Valerie ;

Grose, David ;

Gunthorpe, Martin J. ;

Chessell, Iain P. ;

Tate, Simon ;

Green, Paula J. ;

Woolf, Clifford J. .

JOURNAL OF NEUROSCIENCE, 2006, 26 (50) :12852-12860

[6] GTP-induced tetrodotoxin-resistant Na+ current regulates excitability in mouse and rat small diameter sensory neurones [J].

Baker, MD ;

Chandra, SY ;

Ding, YN ;

Waxman, SG ;

Wood, JN .

JOURNAL OF PHYSIOLOGY-LONDON, 2003, 548 (02) :373-382

[7] DIFFERENTIAL REGULATION OF 3 SODIUM-CHANNEL MESSENGER-RNAS IN THE RAT CENTRAL NERVOUS-SYSTEM DURING DEVELOPMENT [J].

BECKH, S ;

NODA, M ;

LUBBERT, H ;

NUMA, S .

EMBO JOURNAL, 1989, 8 (12) :3611-3616

[8] Two TTX-resistant Na+ currents in mouse colonic dorsal root ganglia neurons and their role in colitis-induced hyperexcitability [J].

Beyak, MJ ;

Ramji, N ;

Krol, KM ;

Kawaja, MD ;

Vanner, SJ .

AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2004, 287 (04) :G845-G855

[9] Mild gastritis alters voltage-sensitive sodium currents in gastric sensory neurons in rats [J].

Bielefeldt, K ;

Ozaki, N ;

Gebhart, GF .

GASTROENTEROLOGY, 2002, 122 (03) :752-761

[10] Nociceptors Are Interleukin-1β Sensors [J].

Binshtok, Alexander M. ;

Wang, Haibin ;

Zimmermann, Katharina ;

Amaya, Fumimasa ;

Vardeh, Daniel ;

Shi, Lin ;

Brenner, Gary J. ;

Ji, Ru-Rong ;

Bean, Bruce P. ;

Woolf, Clifford J. ;

Samad, Tarek A. .

JOURNAL OF NEUROSCIENCE, 2008, 28 (52) :14062-14073

← 1 2 3 4 5 6 7 8 9 10 →