| pubmed-article:10529720 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10529720 | lifeskim:mentions | umls-concept:C0085979 | lld:lifeskim |
| pubmed-article:10529720 | lifeskim:mentions | umls-concept:C0064239 | lld:lifeskim |
| pubmed-article:10529720 | lifeskim:mentions | umls-concept:C0086376 | lld:lifeskim |
| pubmed-article:10529720 | lifeskim:mentions | umls-concept:C0205753 | lld:lifeskim |
| pubmed-article:10529720 | lifeskim:mentions | umls-concept:C0206473 | lld:lifeskim |
| pubmed-article:10529720 | lifeskim:mentions | umls-concept:C0019409 | lld:lifeskim |
| pubmed-article:10529720 | lifeskim:mentions | umls-concept:C2603343 | lld:lifeskim |
| pubmed-article:10529720 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:10529720 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
| pubmed-article:10529720 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:10529720 | pubmed:dateCreated | 1999-11-30 | lld:pubmed |
| pubmed-article:10529720 | pubmed:abstractText | There is strong evidence supporting the existence of multiple kappa receptors. Previous studies proposed that U69,593 and (+)-tifluadom act on different kappa receptor subtypes, kappa(1) (kappa(1)) and kappa(2) (kappa(2)), respectively. In this study, we investigated the effects of the kappa selective antagonist nor-binaltorphimine (Nor-BNI) on U69,593- and (+)-tifluadom-induced receptor-mediated stimulation of [(35)S]-GTP-gamma-S binding in the guinea pig caudate. The IC(50) value of Nor-BNI in the presence of a stimulating concentration of U69,593 (1 microM) was 0.19+/-0.02; while the IC(50) for Nor-BNI in the presence of (+)-tifluadom (1 microM) was 13.9+/- 1.62 nM. The mu-opioid receptor antagonist CTAP (10,000 nM) significantly reduced (+)-tifluadom-stimulated [(35)S]-GTP-gamma-S binding in rat brain sections and guinea pig brain membranes, indicating that (+)-tifluadom has mu agonist activity. Under conditions in which the mu agonist activity of (+)-tifluadom was blocked by 1000 nM CTAP the Ki value for Nor-BNI for inhibition of U69,593-stimulated [(35)S]-GTP-gamma-S binding was 0.036+/-.004 nM, whereas, its Ki value for the (+)-tifluadom-stimulated [(35)S]-GTP-gamma-S binding was 0.27+/-.015 nM. These results suggest that (+)-tifluadom and U69,593 activate pharmacologically different receptors. This study provides functional evidence in support of kappa receptor heterogeneity. | lld:pubmed |
| pubmed-article:10529720 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10529720 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10529720 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10529720 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10529720 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:10529720 | pubmed:issn | 0887-4476 | lld:pubmed |
| pubmed-article:10529720 | pubmed:author | pubmed-author:RiceK CKC | lld:pubmed |
| pubmed-article:10529720 | pubmed:author | pubmed-author:JacksonCC | lld:pubmed |
| pubmed-article:10529720 | pubmed:author | pubmed-author:RothmanR BRB | lld:pubmed |
| pubmed-article:10529720 | pubmed:author | pubmed-author:HeyligerS OSO | lld:pubmed |
| pubmed-article:10529720 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10529720 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:10529720 | pubmed:volume | 34 | lld:pubmed |
| pubmed-article:10529720 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10529720 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10529720 | pubmed:pagination | 256-65 | lld:pubmed |
| pubmed-article:10529720 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:10529720 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10529720 | pubmed:articleTitle | Opioid peptide receptor studies. 10. Nor-BNI differentially inhibits kappa receptor agonist-induced G-protein activation in the guinea pig caudate: further evidence of kappa receptor heterogeneity. | lld:pubmed |
| pubmed-article:10529720 | pubmed:affiliation | Clinical Psychopharmacology Section, Division of Intramural Research, National Institute on Drug Abuse, National Institutes of Health, P. O. Box 5180, 5500 Nathan Shock Drive, Baltimore, MD 21224, USA. | lld:pubmed |
| pubmed-article:10529720 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10529720 | pubmed:publicationType | In Vitro | lld:pubmed |
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