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Titolo:
Plasticity of sodium channel expression in DRG neurons in the chronic constriction injury model of neuropathic pain
Autore:
Dib-Hajj, SD; Fjell, J; Cummins, TR; Zheng, Z; Fried, K; LaMotte, R; Black, JA; Waxman, SG;
Indirizzi:
Yale Univ, Sch Med, Dept Neurol, New Haven, CT 06510 USA Yale Univ New Haven CT USA 06510 ed, Dept Neurol, New Haven, CT 06510 USA Vet Affairs Med Ctr, PVA, EPVA Neurosci Res Ctr, W Haven, CT 06516 USA VetAffairs Med Ctr W Haven CT USA 06516 i Res Ctr, W Haven, CT 06516 USA Vet Affairs Med Ctr, Rehabil Res Ctr, W Haven, CT 06516 USA Vet Affairs Med Ctr W Haven CT USA 06516 l Res Ctr, W Haven, CT 06516 USA Karolinska Inst, Dept Neurosci, SE-17177 Stockholm, Sweden Karolinska Inst Stockholm Sweden SE-17177 ci, SE-17177 Stockholm, Sweden Yale Univ, Sch Med, Dept Anesthesiol, New Haven, CT 06510 USA Yale Univ New Haven CT USA 06510 ept Anesthesiol, New Haven, CT 06510 USA
Titolo Testata:
PAIN
fascicolo: 3, volume: 83, anno: 1999,
pagine: 591 - 600
SICI:
0304-3959(199912)83:3<591:POSCEI>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
DORSAL-ROOT GANGLION; SPINAL SENSORY NEURONS; SCIATIC-NERVE INJURY; PERIPHERAL NEUROPATHY; GENE-EXPRESSION; MESSENGER-RNA; NA+ CHANNEL; RAT MODEL; WALLERIAN DEGENERATION; DOWN-REGULATION;
Keywords:
TTX-R Na current; rapidly repriming Na current; thermal hyperalgesia; RT-PCR; in situ hybridization;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Waxman, SG Yale Univ, Sch Med, Dept Neurol, LCI 707,333 Cedar St, New Haven, CT 06510USA Yale Univ LCI 707,333 Cedar St New Haven CT USA 06510 06510USA
Citazione:
S.D. Dib-Hajj et al., "Plasticity of sodium channel expression in DRG neurons in the chronic constriction injury model of neuropathic pain", PAIN, 83(3), 1999, pp. 591-600

Abstract

Previous studies have shown that transection of the sciatic nerve induces dramatic changes in sodium currents of axotomized dorsal root ganglion (DRG) neurons, which are paralleled by significant changes in the levels of transcripts of several sodium channels expressed in these neurons. Sodium currents that are resistant to tetrodotoxin (TTX-R) and the transcripts of two TTX-R sodium channels are significantly attenuated, while a rapidly repriming tetrodotoxin-sensitive (TTX-S) current emerges and the transcripts of alpha-III sodium channel, which produce a TTX-S current when expressed in oocytes, are up-regulated. We report here on changes in sodium currents and sodium channel transcripts in DRG neurons in the chronic constriction injury (CCI) model of neuropathic pain. CCI-induced changes in DRG neurons, 14 days post-surgery, mirror those of axotomy. Transcripts of NaN and SNS, two sensory neuron-specific TTX-R sodium channels, are significantly down-regulated as is the TTX-R sodium current, while transcripts of the TTX-S alpha-IIIsodium channel and a rapidly repriming TTX-S Na current are up-regulated in small diameter DRG neurons. These changes may provide at least a partial basis for the hyperexcitablity of DRG neurons that contributes to hyperalgesia in this model. (C) 1999 International Association for the Study of Pain. Published by Elsevier Science B.V.

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Documento generato il 30/11/20 alle ore 03:09:32