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Narita, M, Aoki, T, Ozaki, S, Yajima, Y and Suzuki, T (2001) Involvement of protein kinase Cgamma isoform in morphine-induced reinforcing effects. Neuroscience 103:309-14


The present study was designed to investigate the role of protein kinase C (PKC) isoform in the morphine-induced reinforcing effect in mice. An intracerebroventricular injection of calphostin C, a specific PKC inhibitor, produced a dose-dependent reduction in the morphine-induced place preference. The protein level of PKCgamma was significantly up-regulated in membrane preparations of the limbic forebrain obtained from the morphine-conditioned mice compared to that from the saline-conditioned mice. However, the protein levels of PKCalpha, betaI, betaII and epsilon were not affected in the same preparation. By contrast, there were no changes in the protein level of all five PKC isoforms in the lower midbrain. Furthermore, we investigated the rewarding properties of morphine in mice lacking PKCgamma gene. A significant place preference was observed following treatment with morphine in wild-type mice, whereas such an effect of morphine was not found in PKCgamma knockout mice. These findings suggest that activated PKCgamma in the limbic forebrain following the treatment with morphine may be critical for the development and/or maintenance of reinforcing effects induced by morphine in mice.




Analgesics, Opioid/pharmacology; Animals; Conditioning (Psychology)/drug effects; Dose-Response Relationship, Drug; Isoenzymes/genetics; Isoenzymes/metabolism; Limbic System/drug effects; Limbic System/enzymology; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Morphine/pharmacology; Morphine Dependence/metabolism; Protein Kinase C/genetics; Protein Kinase C/metabolism; Reinforcement (Psychology); Reward



Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status



GO:0043278: response to morphine

ECO:0000315: mutant phenotype evidence used in manual assertion


Seeded From UniProt


See also


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