pubmed-article:1611514 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1611514 | lifeskim:mentions | umls-concept:C0026549 | lld:lifeskim |
pubmed-article:1611514 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
pubmed-article:1611514 | lifeskim:mentions | umls-concept:C0814083 | lld:lifeskim |
pubmed-article:1611514 | lifeskim:mentions | umls-concept:C0243076 | lld:lifeskim |
pubmed-article:1611514 | lifeskim:mentions | umls-concept:C0392760 | lld:lifeskim |
pubmed-article:1611514 | pubmed:issue | 1-2 | lld:pubmed |
pubmed-article:1611514 | pubmed:dateCreated | 1992-7-24 | lld:pubmed |
pubmed-article:1611514 | pubmed:abstractText | In the present study we have examined the interaction between the selective cholecystokinin (CCK)A and CCKB receptor antagonists, devazepide and L365-260 on morphine conditioned place preference (CPP). Using an unbiased procedure, morphine (1.5 mg/kg) produced a reliable CPP which was observed irrespective of the conditioning compartment type. Pretreatment with devazepide (0.001-0.01 mg/kg s.c.) produced a dose related attenuation of this response. At higher doses (0.1-1 mg/kg) this antagonism became variable and dependent on the training compartment with blockade only observed when conditioning was to the white/rough textured environment. This profile has also been reported for the serotonin (5-HT)3 receptor antagonist ondansetron. The CCKB antagonist L365-260 (0.000001-0.01 mg/kg) failed to antagonize the morphine CPP, if anything a mild potentiation was observed. To study this further we examined the interaction between L365-260 (0.01 mg/kg) and a subthreshold dose of morphine (0.3 mg/kg). At these doses neither drug elicited CPP, however when co-administered a significant CPP was recorded. Finally, L365-260 at 1 mg/kg induced a mild but significant CPP when administered alone. These results suggest a differential role of CCK receptor subtypes on reward-related behaviour and complement previous studies suggesting bimodal effects of CCK systems on mesolimbic dopamine function. | lld:pubmed |
pubmed-article:1611514 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1611514 | pubmed:language | eng | lld:pubmed |
pubmed-article:1611514 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1611514 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:1611514 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1611514 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1611514 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1611514 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1611514 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1611514 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1611514 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1611514 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1611514 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1611514 | pubmed:month | Feb | lld:pubmed |
pubmed-article:1611514 | pubmed:issn | 0006-8993 | lld:pubmed |
pubmed-article:1611514 | pubmed:author | pubmed-author:SellersE MEM | lld:pubmed |
pubmed-article:1611514 | pubmed:author | pubmed-author:HigginsG AGA | lld:pubmed |
pubmed-article:1611514 | pubmed:author | pubmed-author:NguyenPP | lld:pubmed |
pubmed-article:1611514 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1611514 | pubmed:day | 14 | lld:pubmed |
pubmed-article:1611514 | pubmed:volume | 572 | lld:pubmed |
pubmed-article:1611514 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1611514 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1611514 | pubmed:pagination | 208-15 | lld:pubmed |
pubmed-article:1611514 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:1611514 | pubmed:year | 1992 | lld:pubmed |
pubmed-article:1611514 | pubmed:articleTitle | Morphine place conditioning is differentially affected by CCKA and CCKB receptor antagonists. | lld:pubmed |
pubmed-article:1611514 | pubmed:affiliation | Clinical Psychopharmacology Program, Addiction Research Foundation, Toronto, Ontario, Canada. | lld:pubmed |
pubmed-article:1611514 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1611514 | pubmed:publicationType | Comparative Study | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1611514 | lld:pubmed |