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Titolo:
EFFECTS OF MU-OPIOID-RECEPTOR AND DELTA-OPIOID-RECEPTOR ANTAGONISTS ON THE STIMULUS PROPERTIES OF CHOLECYSTOKININ
Autore:
RILEY AL; MELTON PM;
Indirizzi:
AMERICAN UNIV,DEPT PSYCHOL,PSYCHOPHARMACOL LAB WASHINGTON DC 20016
Titolo Testata:
Pharmacology, biochemistry and behavior
fascicolo: 1-2, volume: 57, anno: 1997,
pagine: 57 - 62
SICI:
0091-3057(1997)57:1-2<57:EOMADA>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
PREVENTS MORPHINE-TOLERANCE; CONDITIONED TASTE-AVERSION; OBESE FA/FA RATS; ZUCKER LEAN FA/; B RECEPTOR; INDUCED ANALGESIA; BETA-ENDORPHIN; SELECTIVE ANTAGONIST; PLACE PREFERENCE; SQUIRREL-MONKEY;
Keywords:
CCK; NALOXONE; NALTRINDOLE; DRUG DISCRIMINATION LEARNING; OPIOID ANTAGONISM; MU; DELTA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
80
Recensione:
Indirizzi per estratti:
Citazione:
A.L. Riley e P.M. Melton, "EFFECTS OF MU-OPIOID-RECEPTOR AND DELTA-OPIOID-RECEPTOR ANTAGONISTS ON THE STIMULUS PROPERTIES OF CHOLECYSTOKININ", Pharmacology, biochemistry and behavior, 57(1-2), 1997, pp. 57-62

Abstract

Melton and Riley recently reported that the relatively selective mu-opioid-antagonist naloxone potentiated the stimulus properties of the gut peptide cholecystokinin (CCK). To assess whether such opioid potentiation is limited to activity at the mu-receptor subtype, in the present experiment the effects of the highly selective delta-antagonist naltrindole on CCK's stimulus properties were examined. Because in the initial report of naloxone's potentiation of CCK a relatively high, nonphysiologic dose of CCK (i.e., 13 mu g/kg) was used as the training drug, in the current analysis subjects were trained to discriminate 5.6 mu g/kg CCK from its vehicle and the assessments and comparisons of theeffects of naloxone and naltrindole were based on this dose. Specifically, rats were administered 5.6 mu g/kg CCK before saccharin-LiCl pairings and the CCK vehicle before saccharin alone. With such training, they rapidly acquired the drug discrimination, avoiding saccharin consumption when it was preceded by CCK and consuming the same saccharin solution when it was preceded by its vehicle. In subsequent generalization tests, doses of CCK that were ineffective in suppressing saccharinconsumption (i.e., did not substitute for the training dose of CCK) did result in the suppression of saccharin consumption when combined with doses of the mu antagonist naloxone that alone had no effect on saccharin intake. On the other hand, the highly selective delta-opioid-receptor antagonist naltrindole was ineffective in potentiating the effects of CCK. Specifically, when naltrindole was combined with ineffective doses of CCK, subjects drank at control levels. The ability of naloxone to potentiate CCK's stimulus effects is consistent with a range of other demonstrations of the role of the mu-opioid-receptor subtype in CCK-opioid interactions, although the specific basis for the interaction remains unknown. Given recent findings on the effects of delta agonists and antagonists on CCK-induced activity, the failure of naltrindole to potentiate CCK's stimulus effects may be due to the absence ofdelta activity within this preparation, rather than the absence of delta mediation of CCK-opioid interactions in general. (C) 1997 ElsevierScience Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/04/20 alle ore 00:22:23