RhoA/ROCK pathway mediates morphological changes downstream of P2Y12/13 receptors in spinal microglia following peripheral nerve injury
Project/Area Number |
24500416
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Nerve anatomy/Neuropathology
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Research Institution | Hyogo Medical University |
Principal Investigator |
|
Co-Investigator(Renkei-kenkyūsha) |
YAMANAKA Hiroki 兵庫医科大学, 医学部, 講師 (20340995)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | マイクログリア / ATP受容体 / MAP kinase / Rho kinase / 脊髄後角 / 神経障害性疼痛 / 形態変化 / ADP / P2Y受容体 / p38 MAPK |
Outline of Final Research Achievements |
Recent studies have indicated an important role of ATP receptors in spinal microglia, such as P2Y12 or P2Y13, in the development of chronic pain. However, intracellular signaling cascade of these receptors have not been clearly elucidated. We found that P2Y12 and P2Y13 receptors could activate Rho/ROCK and contribute to pathological changes in activated spinal microglia after nerve injury, moreover Rho kinase inhibitor significantly inhibited the injury-induced tactile allodynia.
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Report
(4 results)
Research Products
(4 results)