Up-regulation of mu-opioid receptor-mediated G-protein activation in protein kinase Cgamma knockout mice following repeated naloxone treatment.
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Narita M, Suzuki M, Mizoguchi H, Narita M, Yajima Y, Sakurada S, Tseng LF, Suzuki T
Up-regulation of mu-opioid receptor-mediated G-protein activation in protein kinase Cgamma knockout mice following repeated naloxone treatment.
Neurosci Lett. 2003 Feb 27;338(2):103-6.
- PubMed ID
- 12566163 [ View in PubMed]
- Abstract
The aim of the present study was to investigate whether repeated treatment with the mu-opioid receptor antagonist naloxone could affect G-protein activation induced by a selective mu-opioid receptor agonist [D-Ala(2),N-MePhe(4),Gly-ol(5)]enkephalin (DAMGO) in mice lacking the protein kinase Cgamma isoform monitoring guanosine-5'-o-(3-[(35)S]thio)triphosphate ([(35)S]GTPgammaS) binding. Repeated s.c. administration of naloxone for 7 days resulted in a significant enhancement of the increased [(35)S]GTPgammaS binding by DAMGO to membranes of the spinal cord obtained from mice lacking the protein kinase Cgamma isoform. Furthermore, immunoreactivities of membrane-located protein kinase Cgamma and phosphorylated-protein kinase C in the spinal cord of ICR mice were not altered by repeated naloxone treatment. The present data provide direct evidence that protein kinase Cgamma is not involved in the development of the up-regulation of mu-opioid receptor functions to activate G-proteins in the mouse spinal cord by repeated naloxone treatment.
DrugBank Data that Cites this Article
- Drug Targets
Drug Target Kind Organism Pharmacological Action Actions Naloxone Mu-type opioid receptor Protein Humans YesAntagonistDetails