The expression of G protein-coupled receptor 3 modulates presynaptic function in differentiated PC12 cells
| Project/Area Number |
18K07392
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 51030:Pathophysiologic neuroscience-related
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| Research Institution | Hiroshima University |
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Principal Investigator |
Tanaka Shigeru 広島大学, 医系科学研究科(医), 講師 (20512651)
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| Co-Investigator(Kenkyū-buntansha) |
細見 直永 広島大学, 原爆放射線医科学研究所, 研究員 (70363190)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | GPR3 / シナプシン / 神経細胞 / プレシナプス / PKA / cAMP / PC12細胞 / Synapsin / 海馬神経細胞 / 軸索再生 |
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| Outline of Final Research Achievements |
G-protein coupled receptor (GPR) 3 belongs to a member of constitutively active Gs-coupled receptors that activate 3', -5'-cyclic adenosine monophosphate (cAMP). We have previously reported that the neuronal expression of GPR3 enhances neurite outgrowth, modulates proliferation of cerebellar granule cell precursors, and associates with neuronal survival. Recently, we clarified that the subcellular dynamics of GPR3 are associated with local activation of PKA in cerebellar granular neurons. In the present study, we aimed to determine the possible involvement of GPR3 in presynaptic function using PC12 cells. We clarified that intrinsic expression of GPR3 plays a role in the induction of synapsin2 and further effect on the phosphorylation of synapsin. Therefore, GPR3 may serve as a potential modulator of presynaptic function.
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| Academic Significance and Societal Importance of the Research Achievements |
研究代表者はこれまで神経細胞におけるGPR3の局在・機能・役割に関した基礎的研究を続けてきた。GPR3はアルツハイマー病においてBACE１の修飾因子として病態に関与する可能性が報告されているが、シナプス形成機能に関しての報告はこれまでになく、将来の神経再生医療の基礎となる可能性があり、学術的にも意義がある研究課題であると考えられる。
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Report
(4 results)
Research Products
(46 results)
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[Journal Article] Syntaxin 3 interacts with serotonin transporter and regulates its function.2021
Author(s)
Motoike, S., Taguchi, K., Harada, K., Asano, M., Hide, I. Tanaka, S. Irifune, M. and Sakai,
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Journal Title
J. Pharmacol. Sci.
Volume: 145
Issue: 4
Pages: 297-307
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Component of nicotine-induced intracellular calcium elevation mediated throughα3- andα5-containing nicotinic acetylcholine receptors are regulated by cyclic AMP in SH-SY 5Y cells2020
Author(s)
Takahashi, T., Yoshida, T., Harada, K., Miyagi, T., Hashimoto, K., Hide, I., Tanaka, S., Irifune, M. and Sakai, N.
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Journal Title
PLos One
Volume: 15
Issue: 11
Pages: e0242349-e0242349
DOI
Related Report
Peer Reviewed / Open Access
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[Book] 脳卒中病態学のススメ2018
Author(s)
下畑享良編集 田中茂（分担執筆）
Total Pages
354
Publisher
南山堂
ISBN
9784525248512
Related Report
