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Titolo:
ATTENUATION OF WITHDRAWAL-INDUCED HYPERACTIVITY OF LOCUS-COERULEUS NEURONS BY INHIBITORS OF NITRIC-OXIDE SYNTHASE IN MORPHINE-DEPENDENT RATS
Autore:
PINEDA J; TORRECILLA M; MARTINRUIZ R; UGEDO L;
Indirizzi:
UNIV BASQUE COUNTRY,FAC MED,DEPT PHARMACOL,BARRIO SARRIENA S-N E-48940 LEIOA VIZCAYA SPAIN
Titolo Testata:
Neuropharmacology
fascicolo: 6, volume: 37, anno: 1998,
pagine: 759 - 767
SICI:
0028-3908(1998)37:6<759:AOWHOL>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
NALOXONE-PRECIPITATED WITHDRAWAL; OPIATE WITHDRAWAL; NORADRENERGIC NEURONS; OPIOID WITHDRAWAL; 7-NITRO INDAZOLE; BRAIN; CERULEUS; EXPRESSION; ACTIVATION; TOLERANCE;
Keywords:
MORPHINE; OPIATE WITHDRAWAL; OPIATE DEPENDENCE; LOCUS COERULEUS; NITRIC OXIDE SYNTHASE INHIBITOR; ELECTROPHYSIOLOGY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
47
Recensione:
Indirizzi per estratti:
Citazione:
J. Pineda et al., "ATTENUATION OF WITHDRAWAL-INDUCED HYPERACTIVITY OF LOCUS-COERULEUS NEURONS BY INHIBITORS OF NITRIC-OXIDE SYNTHASE IN MORPHINE-DEPENDENT RATS", Neuropharmacology, 37(6), 1998, pp. 759-767

Abstract

Electrophysiological, biochemical, and behavioural studies have suggested that opiate withdrawal is mediated, at least in part, by a hyperactivity of locus coeruleus (LC) neurones. The aim of this study was toevaluate, using single-unit extracellular recordings, the role of NO in the opiate withdrawal-induced hyperactivity of LC neurones in anaesthetized rats. In animals chronically treated with morphine (5 days), administration of naloxone caused an increase in the spontaneous firing rate of LC cells. Acute pretreatment with the nitric oxide synthase (NOS) inhibitor N-G-nitro-L-arginine methyl ester (30 mg kg(-1) i.p.) attenuated some signs of opiate withdrawal (total score reduced by 55%), and also the withdrawal-induced hyperactivity of LC neurones (hyperactivity reduced by similar to 50%). Acute pretreatment with 7-nitro indazole (50 mg kg(-1) i.p.), a selective inhibitor of neuronal NOS, caused a complete blockade of the withdrawal-induced hyperactivity of LCneurones. Application of 7-nitro indazole (30 mu M) in the vicinity of the LC also caused a reduction (of similar to 60%) in the withdrawal-induced hyperactivity of LC cells. Intravenous administration of these NOS inhibitors (after naloxone challenge) did not produce comparablechanges in the LC cell firing activity. 7-Nitro indazole failed to affect the development of tolerance of the LC to the morphine effect in opiate-dependent rats (i.e. morphine dose-effect curves were shifted to the right by morphine treatments to a similar degree in vehicle- and7-nitro indazole-pretreated rats). The present data suggest that opiate withdrawal might be mediated by nitric oxide acting as an intermediate messenger in the LC. (C) 1998 Elsevier Science Ltd. All rights reserved.

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Documento generato il 02/04/20 alle ore 19:28:47