| First Author | Tsu RC | Year | 1995 |
| Journal | J Neurochem | Volume | 64 |
| Issue | 6 | Pages | 2700-7 |
| PubMed ID | 7760050 | Mgi Jnum | J:25551 |
| Mgi Id | MGI:73267 | Doi | 10.1046/j.1471-4159.1995.64062700.x |
| Citation | Tsu RC, et al. (1995) Regulation of multiple effectors by the cloned delta-opioid receptor: stimulation of phospholipase C and type II adenylyl cyclase. J Neurochem 64(6):2700-7 |
| abstractText | The delta-opioid receptor is known to regulate multiple effectors in various tissues. When expressed in human embryonic kidney 293 cells, the cloned delta-opioid receptor inhibited cyclic AMP (cAMP) accumulation in response to the delta-selective agonist [D-Pen2,D-Pen5]-enkephalin. The inhibitory response of [D-Pen2,D-Pen5]-enkephalin was dependent on the expression of the delta-opioid receptor and exhibited an EC50 of 1 nM. The receptor showed ligand selectivity and a pharmacological profile that is appropriate for the delta-opioid subtype. The inhibition was blocked by the opiate antagonist naloxone or by pretreatment of the cells with pertussis toxin. Co-transfection of the delta-opioid receptor with type II adenylyl cyclase and an activated mutant of alpha s converted the delta-opioid signal from inhibition to stimulation of cAMP accumulation. It is interesting that when transfected into Ltk-fibroblasts, the cloned delta-opioid receptor was able to stimulate the formation of inositol phosphates (EC50 = 8 nM). This response was sensitive to pertussis toxin. The opioid-mediated formation of inositol phosphates exhibited the same ligand selectivity as seen with the inhibition of cAMP accumulation. The ability of the delta-opioid receptor to couple to G proteins other than Gi was also examined. Cotransfection studies revealed that the delta-opioid receptor can utilize Gz to regulate cAMP accumulation and to stimulate the formation of inositol phosphates. |
