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Titolo:
INVOLVEMENT OF CALCIUM AND L-TYPE CHANNELS IN NICOTINE-INDUCED ANTINOCICEPTION
Autore:
DAMAJ MI; WELCH SP; MARTIN BR;
Indirizzi:
VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PHARMACOL & TOXICOLRICHMOND VA 23298 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PHARMACOL & TOXICOLRICHMOND VA 23298
Titolo Testata:
The Journal of pharmacology and experimental therapeutics
fascicolo: 3, volume: 266, anno: 1993,
pagine: 1330 - 1338
SICI:
0022-3565(1993)266:3<1330:IOCALC>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
GENE-RELATED PEPTIDE; ACETYLCHOLINE-RECEPTOR; CORTICAL SYNAPTOSOMES; INTRATHECAL MORPHINE; SUBSTANCE-P; ANTAGONISTS; CELLS; RELEASE; RAT; STIMULATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
54
Recensione:
Indirizzi per estratti:
Citazione:
M.I. Damaj et al., "INVOLVEMENT OF CALCIUM AND L-TYPE CHANNELS IN NICOTINE-INDUCED ANTINOCICEPTION", The Journal of pharmacology and experimental therapeutics, 266(3), 1993, pp. 1330-1338

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 calcium ion fluxes in the response to nicotine on a cellular level. Alteration of nicotine-induced antinociception in mice after systemic administration was therefore investigated in the presence of several drugs that increase intracellular calcium. Calcium, (+/-)-BAYK 8644, thapsigargin, glyburide and A23187 administered intrathecally (i.t.) were found to enhance nicotine-induced antinociception by shifting its dose-response curve to the left. Conversely, i.t. administration of agents which decrease intracellular calcium, such as EGTA and alpha-calcitonin gene-related peptide, blocked nicotine-induced antinociception. These findings support a role for spinal intracellular calcium in the pharmacological effects of nicotine. Additionally, blockade of antinociception by nimodipine and nifedipine indicates that a L-type calcium channel is involved in nicotine's effect. However, nicotine did not compete for [H-3] nitrendipine binding. Intrathecal administration of mecamylamine, a nicotinic antagonist, resulted in a blockade of antinociception produced by the i.t. injection of thapsigargin, A23187, calcium and (+/-)-BAYK 8644. The mechanism ofmecamylamine's antagonism of nicotine is uncertain. However, these results suggest that mecamylamine blocks the effects of drugs which increase intracellular calcium by either a modulation of intracellular calcium-dependent mechanisms or a blockade of calcium channels. Thus, mecamylamine could modulate a calcium signaling process secondary to receptor activation resulting in blockade of antinociception produced by diverse agents.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/09/20 alle ore 09:42:03