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Titolo:
SEVERAL ROLES OF CCKA AND CCKB RECEPTOR SUBTYPES IN CCK-8-INDUCED ANDLIC1-INDUCED TASTE-AVERSION CONDITIONING
Autore:
MOSHER JT; JOHNSON MF; BIRKEMO LS; ERVIN GN;
Indirizzi:
BRIGHAM YOUNG UNIV,DEPT PSYCHOL,1084 SWKT PROVO UT 84602 GLAXO WELLCOME RES INST,DEPT PHARMACOL RES TRIANGLE PK NC 27709
Titolo Testata:
Peptides
fascicolo: 3, volume: 17, anno: 1996,
pagine: 483 - 488
SICI:
0196-9781(1996)17:3<483:SROCAC>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
DECREASES FOOD-INTAKE; C-TERMINAL OCTAPEPTIDE; RAT VAGUS NERVE; BINDING-SITES; BAIT SHYNESS; CHOLECYSTOKININ; BRAIN; DRUGS; AUTORADIOGRAPHY; ANTAGONISTS;
Keywords:
CCK; CCK-8; DEVAZEPIDE; MK-329; L-364,718; L-365,260; CL-988; LICL; CHLORDIAZEPOXIDE; HCL; TASTE AVERSION CONDITIONING;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
47
Recensione:
Indirizzi per estratti:
Citazione:
J.T. Mosher et al., "SEVERAL ROLES OF CCKA AND CCKB RECEPTOR SUBTYPES IN CCK-8-INDUCED ANDLIC1-INDUCED TASTE-AVERSION CONDITIONING", Peptides, 17(3), 1996, pp. 483-488

Abstract

Administration of a relatively large IP dose of sulfated cholecystokinin (26-33) (CCK-8; 1.0 mu mol/kg) consistently induced moderate tasteaversion conditioning (TAG) using a 20-min, one-bottle test in Long-Evans rats. Because CCK-8 has affinity for both CCK, and CCK, receptor subtypes, we wanted to determine the subtype involved in CCK-8-inducedTAG. Pretreatment with the selective CCK, antagonist MK-329 (L-364,718 or devazepide), at doses of 0.1, 1.0, or 10.0 mu mol/kg, markedly antagonized (>70%) CCK-8-induced TAG. Pretreatment with the selective CCKB antagonist L-365,260, at doses of 0.1 or 1.0 mu mol/kg, partially antagonized (similar to 50%) CCK-8-induced TAC, although the highest dose of L-365,260, 10.0 mu mol/kg, did not. These partial antagonistic effects of L-365,260 on CCK-8-induced TAC were replicated in our secondstudy. In our third study, we observed that another CCK, antagonist, the dipeptoid CI-988, also partially antagonized CCK-8-induced TAC at a dose of 0.1, but not 1.0 or 10.0, mu mol/kg. In our final study, pretreatments with a single dose (i.e., 10.0, but not 0.1 or 1.0, mu mol/kg) of either MK-329 or L-365,260 were also shown to partially antagonize the formation of moderate TAC induced by treatment with LiCl at 708 mu mol/kg. Marked antagonism of LiCl-induced TAC was also observed following pretreatment with the known anxiolytic chlordiazepoxide HCl at 7.4 mu mol/kg. Considering the existing data on the induction of TACby various CCK analogues, we consider an action of CCK-8 on peripheral CCKA, but not CCKB, receptors necessary for the induction of TAG. Our results of partial antagonism of CCK-8- and LiCl-induced TAC by L-365,260, CI-988, or MK-329 suggest, but do not prove, that both CCK, andCCKB mechanisms may be operative during TAG. Because the CCK antagonists affected TAC like chlordiazepoxide, blockade of CCK, and CCK, mechanisms may produce a mild anxiolytic effect.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 20:23:28