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Titolo:
The involvement of spinal Ca2+/calmodulin-protein kinase II in nicotine-induced antinociception in mice
Autore:
Damaj, MI;
Indirizzi:
Virginia Commonwealth Univ, Med Coll Virginia, Dept Pharmacol & Toxicol, Richmond, VA 23298 USA Virginia Commonwealth Univ Richmond VA USA 23298 , Richmond, VA 23298 USA
Titolo Testata:
EUROPEAN JOURNAL OF PHARMACOLOGY
fascicolo: 1-2, volume: 404, anno: 2000,
pagine: 103 - 110
SICI:
0014-2999(20000915)404:1-2<103:TIOSCK>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
NUCLEUS RAPHE MAGNUS; ACETYLCHOLINE-RECEPTORS; ALPHA-BUNGAROTOXIN; NERVOUS-SYSTEM; BINDING-SITES; INHIBITOR; RAT; NEURONS; CALCIUM; CELLS;
Keywords:
nicotine; antinociception; CaM kinase II; (mice); Ca2+ channels; intrathecal;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Damaj, MI Virginia Commonwealth Univ, Med Coll Virginia, Dept Pharmacol & Toxicol, Box 980613, Richmond, VA 23298 USA Virginia Commonwealth Univ Box 980613 Richmond VA USA 23298 USA
Citazione:
M.I. Damaj, "The involvement of spinal Ca2+/calmodulin-protein kinase II in nicotine-induced antinociception in mice", EUR J PHARM, 404(1-2), 2000, pp. 103-110

Abstract

The nature of the signaling process activated by neuronal nicotinic receptors has not been Fully defined; however, several recent studies have implicated the involvement of Ca2+ fluxes in the response to nicotine. In order to assess Ca2+-dependent mechanisms in nicotine-induced antinociception, theCa2+ channel antagonist nimodipine and several calcium/calmodulin-protein kinase II (CaM kinase II) inhibitors were evaluated for their effects on nicotine-induced antinociception. The results indicate that both of these antagonists dose-dependently blocked nicotine-induced antinociception after intrathecal (i.t.) injection. Indeed, three structurally unrelated CaM kinaseII inhibitors blocked nicotine's effects in the tail-flick test in a dose-related manner. A second series of experiments assessed the effect of acutenicotine exposure on [Ca2+](i) and CaM kinase II activity in spinal cord tissues. Nicotine increased [Ca2+](i) in a concentration-dependent manner after application of the drug to spinal synaptosomes. Furthermore, a dose-dependent increase in the spinal cord membrane CaM kinase II activity was seenafter acute injection of nicotine in mice. Taken together, these results are consistent with the hypothesis that nicotine binding to nicotinic receptors leads to channel opening and depolarization responses with an influx ofCa2+ ions, which would reach sufficient levels to activate Ca2+-dependent/CaM kinase II. Neuronal Ca2+ acting via Ca2+-dependent CaM kinase IT, appears to mediate nicotine-induced antinociception at the spinal level. (C) 2000 Elsevier Science B.V. All rights reserved.

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Documento generato il 22/09/20 alle ore 16:17:29