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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Shioda, Norifumi Shirao, Tomoaki Sawai, Masahiro Ishizuka, Yuta Fukunaga, Kohji |
| Description | Author Affiliation: Shioda N ( From the Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, 980-8578, Japan and shioda@m.tohoku.ac.jp.); Sawai M ( From the Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, 980-8578, Japan and.); Ishizuka Y ( the Department of Neurobiology and Behavior, Gunma University Graduate School of Medicine, Maebashi 371-8511, Japan.); Shirao T ( the Department of Neurobiology and Behavior, Gunma University Graduate School of Medicine, Maebashi 371-8511, Japan.); Fukunaga K ( From the Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, 980-8578, Japan and kfukunaga@m.tohoku.ac.jp.) |
| Abstract | We have reported previously that dopamine D2 receptor stimulation activates calcium/calmodulin-dependent protein kinase II (CaMKII) δ3, a CaMKII nuclear isoform, increasing BDNF gene expression. However, the mechanisms underlying that activity remained unclear. Here we report that CaMKIIδ3 is dephosphorylated at Ser(332) by protein phosphatase 1 (PP1), promoting CaMKIIδ3 nuclear translocation. Neuro-2a cells transfected with CaMKIIδ3 showed cytoplasmic and nuclear staining, but the staining was predominantly nuclear when CaMKIIδ3 was coexpressed with PP1. Indeed, PP1 and CaMKIIδ3 coexpression significantly increased nuclear CaMKII activity and enhanced BDNF expression. In support of this idea, chronic administration of the dopamine D2 receptor partial agonist aripiprazole increased PP1 activity and promoted nuclear CaMKIIδ3 translocation and BDNF expression in the rat brain substantia nigra. Moreover, aripiprazole treatment enhanced neurite extension and inhibited cell death in cultured dopaminergic neurons, effects blocked by PP1γ knockdown. Taken together, nuclear translocation of CaMKIIδ3 following dephosphorylation at Ser(332) by PP1 likely accounts for BDNF expression and subsequent neurite extension and survival of dopaminergic neurons. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 35 |
| Volume Number | 290 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2015-08-28 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Brain-Derived Neurotrophic Factor Genetics Calcium-Calmodulin-Dependent Protein Kinase Type 2 Metabolism Cell Nucleus Dopaminergic Neurons Protein Phosphatase 1 Amino Acid Sequence Animals Aripiprazole Pharmacology Chemistry Drug Effects Cell Survival Cells, Cultured Mice Models, Biological Molecular Sequence Data Neurites Phosphopeptides Phosphorylation Protein Transport RNA, Messenger Rats, Wistar Receptors, Dopamine D2 Agonists Serine Substantia Nigra Research Support, Non-U.S. Gov't Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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