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Titolo:
Sensory neuron-specific sodium channel SNS is abnormally expressed in the brains of mice with experimental allergic encephalomyelitis and humans withmultiple sclerosis
Autore:
Black, JA; Dib-Hajj, S; Baker, D; Newcombe, J; Cuzner, ML; 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 Yale Univ, Sch Med, Paralyzed Vet Amer Eastern Paralyzed Vet Assoc, Neurosci Res Ctr, New Haven, CT 06510 USA Yale Univ New Haven CT USA 06510 eurosci Res Ctr, New Haven, CT 06510 USA Vet Affairs Hosp, Rehabil Res Ctr, W Haven, CT 06516 USA Vet Affairs HospW Haven CT USA 06516 abil Res Ctr, W Haven, CT 06516 USA Univ Coll London, Inst Neurol, Dept Neurochem, London WC1N 3BG, England Univ Coll London London England WC1N 3BG ochem, London WC1N 3BG, England
Titolo Testata:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
fascicolo: 21, volume: 97, anno: 2000,
pagine: 11598 - 11602
SICI:
0027-8424(20001010)97:21<11598:SNSCSI>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
ROOT GANGLION NEURONS; GATED NA CHANNEL; DOWN-REGULATION; MESSENGER-RNA; UP-REGULATION; NERVE INJURY; DRG NEURONS; ADULT-RAT; ALPHA-SNS; CELLS;
Keywords:
demyelinating diseases; gene transcription; ion channels;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
46
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:
J.A. Black et al., "Sensory neuron-specific sodium channel SNS is abnormally expressed in the brains of mice with experimental allergic encephalomyelitis and humans withmultiple sclerosis", P NAS US, 97(21), 2000, pp. 11598-11602

Abstract

Clinical abnormalities in multiple sclerosis (MS) have classically been considered to be caused by demyelination and/or axonal degeneration; the possibility of molecular changes in neurons, such as the deployment of abnormalrepertoires of ion channels that would alter neuronal electrogenic properties, has not been considered. Sensory Neuron-Specific sodium channel SNS displays a depolarized voltage dependence, slower activation and inactivationkinetics, and more rapid recovery from inactivation than classical "fast" sodium channels. SNS is selectively expressed in spinal sensory and trigeminal ganglion neurons within the peripheral nervous system and is not expressed within the normal brain. Here we show that sodium channel SNS mRNA and protein, which are not present within the cerebellum of control mice, are expressed within cerebellar Purkinje cells in a mouse model of MS, chronic relapsing experimental allergic encephalomyelitis. We also demonstrate SNS mRNA and protein expression within Purkinje cells from tissue obtained postmortem from patients with MS, but not in control subjects with no neurological disease. These results demonstrate a change in sodium channel expressionin neurons within the brain in an animal model of MS and in humans with MSand suggest that abnormal patterns of neuronal ion channel expression may contribute to clinical abnormalities such as ataxia in these disorders.

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Documento generato il 20/09/20 alle ore 18:43:46