کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2493795 | 1115528 | 2012 | 8 صفحه PDF | دانلود رایگان |

Protein kinase C (PKC) is involved in intra-cellular signal transduction in various physiological and pathological processes including substance abuse. In the present study, the role of PKC in morphine-induced rewarding memory was investigated using the conditioned place preference (CPP) model. We found a significant translocation of PKCs from cytosol to membrane component in nucleus accumbens (NAc) of morphine-conditioned rats in a dose-dependent manner. The translocation was reduced gradually with the maintenance of morphine-induced CPP. Specifically, the protein level of PKCγ in membrane of the NAc was increased in morphine CPP rats, and decreased during the attenuation of morphine-induced CPP, while the protein level of PKCγ in cytosol of the NAc showed an opposite change. Furthermore, the PKC translocation inhibitor γV5-3 impaired the morphine-induced CPP when microinjected into the NAc. These findings indicated that PKC, especially the γ isoform, is essential for the acquisition and maintenance of morphine-associated reward memory.This article is part of a Special Issue entitled ‘Post-Traumatic Stress Disorder’.
► A translocation of PKCs from cytosol to membrane component in nucleus accumbens of morphine-conditioned rats was showed.
► The level of PKCγ in the membrane was increased in morphine CPP rats.
► The PKCγ in the membrane was decreased with the CPP attenuation, while that in the cytosol showed an opposite change.
► Microinjection of γV5-3, a PKC translocation inhibitor into the nucleus accumbens impaired the expression of morphine CPP.
Journal: Neuropharmacology - Volume 62, Issue 2, February 2012, Pages 959–966