| http://purl.uniprot.org/citations/16914643 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16914643 | http://www.w3.org/2000/01/rdf-schema#comment | "To define the roles of the calmodulin-stimulated adenylyl cyclases (AC1 and AC8) in morphine-induced analgesia, tolerance, physical dependence, and conditioned place preference, we used mice having targeted disruptions of either the AC1 or AC8 genes or both genes [double knockout mice (DKO)]. Mice lacking either AC1 or AC8 genes or DKO did not differ from wild-type mice in short-term antinociceptive responses to morphine measured in the tail-flick analgesia assay. Morphine tolerance that developed immediately within 3 h of morphine administration (10 mg/kg s.c.) was significantly attenuated in DKO mice and AC8 single knockout mice. Tolerance induced continually by daily injections of morphine (10 mg/kg s.c.) was also reduced in DKO mice. In DKO mice continually treated with morphine, there was a significant reduction in withdrawal behaviors, including reduced wet-dog shakes and forepaw tremor after naloxone injection (10 mg/kg i.p.). Morphine produced hyperlocomotion and conditioned place preference in wild-type mice, whereas DKO mice displayed significantly less hyperlocomotion and conditioned place preference. Furthermore, the significant increase in phosphorylated cAMP-response element binding protein (CREB) staining in ventral tegmental area induced by long-term morphine treatment was not evident in DKO mice, suggesting that CREB activation by morphine requires cAMP generated by AC1 and AC8. These results support the hypothesis that calmodulin-stimulated adenylyl cyclases are important mediators of the neuronal responses to morphine."xsd:string |
| http://purl.uniprot.org/citations/16914643 | http://purl.org/dc/terms/identifier | "doi:10.1124/mol.106.025783"xsd:string |
| http://purl.uniprot.org/citations/16914643 | http://purl.uniprot.org/core/author | "Li S."xsd:string |
| http://purl.uniprot.org/citations/16914643 | http://purl.uniprot.org/core/author | "Storm D.R."xsd:string |
| http://purl.uniprot.org/citations/16914643 | http://purl.uniprot.org/core/author | "Chan G.C."xsd:string |
| http://purl.uniprot.org/citations/16914643 | http://purl.uniprot.org/core/author | "Chavkin C."xsd:string |
| http://purl.uniprot.org/citations/16914643 | http://purl.uniprot.org/core/author | "Bruchas M.R."xsd:string |
| http://purl.uniprot.org/citations/16914643 | http://purl.uniprot.org/core/author | "Lee M.L."xsd:string |
| http://purl.uniprot.org/citations/16914643 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
| http://purl.uniprot.org/citations/16914643 | http://purl.uniprot.org/core/name | "Mol Pharmacol"xsd:string |
| http://purl.uniprot.org/citations/16914643 | http://purl.uniprot.org/core/pages | "1742-1749"xsd:string |
| http://purl.uniprot.org/citations/16914643 | http://purl.uniprot.org/core/title | "Calmodulin-stimulated adenylyl cyclase gene deletion affects morphine responses."xsd:string |
| http://purl.uniprot.org/citations/16914643 | http://purl.uniprot.org/core/volume | "70"xsd:string |
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