The expression of G protein-coupled receptor 3 modulates presynaptic function in differentiated PC12 cells

2020 Fiscal Year Final Research Report

• Project/Area Number: 18K07392
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 51030:Pathophysiologic neuroscience-related
• Research Institution: Hiroshima University
• Principal Investigator: Tanaka Shigeru 広島大学, 医系科学研究科(医), 講師 (20512651)
• 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)
• Project Period (FY): 2018-04-01 – 2021-03-31
• Keywords: GPR3

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.

Free Research Field

神経科学、神経薬理学、脳梗塞、神経内科

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。