Shibasaki Masahiro, Kurokawa Kazuhiro, Katsura Masashi, Ohkuma Seitaro
Department of Pharmacology, Kawasaki Medical School, Matsushima, Kurashiki 701-0192, Japan.
Synapse. 2009 May;63(5):365-8. doi: 10.1002/syn.20612.
In this study, we investigated whether PKCgamma could be associated with functional changes of vacuolar protein sorting 34 (Vps34) during morphine treatment using primary cultures of cerebral cortical neurons from mice. The immunoprecipitation analysis showed that p-PKCgamma and Vps34 are present together in molecular complexes. The treatment with morphine increases PKCgamma and Vps34 levels. Phosphorylation of PKCgamma increased Vps34 level. The inhibition of morphine-induced increase in PKCgamma phosphorylation reduced Vps34 level. These results indicates that opioid receptor activation increases PKCgamma phosphorylation in the neurons and, in turn, upregulates Vps34 during short-term treatment with neurons.
在本研究中，我们使用小鼠大脑皮质神经元的原代培养物，研究了蛋白激酶Cγ（PKCγ）是否可能与吗啡治疗期间液泡蛋白分选34（Vps34）的功能变化相关。免疫沉淀分析表明，磷酸化PKCγ（p-PKCγ）和Vps34存在于分子复合物中。吗啡处理可增加PKCγ和Vps34的水平。PKCγ的磷酸化增加了Vps34的水平。抑制吗啡诱导的PKCγ磷酸化增加可降低Vps34的水平。这些结果表明，阿片受体激活可增加神经元中PKCγ的磷酸化，进而在神经元短期治疗期间上调Vps34。
