| Project/Area Number |
17K10939
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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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| Research Field |
Orthopaedic surgery
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
Taniguchi Wataru 和歌山県立医科大学, 医学部, 博士研究員 (20453194)
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| Co-Investigator(Kenkyū-buntansha) |
西尾 尚子 和歌山県立医科大学, 医学部, 特別研究員 (40648359)
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| Project Period (FY) |
2017-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | ドーパミン / 脊髄後角 / パッチクランプ法 / D1-like受容体 / D2-like受容体 / 神経障害性疼痛 / 神経障害性疼痛モデル / 神経科学 |
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| Outline of Final Research Achievements |
The periventricular, posterior region (A11) of the hypothalamus is the principle source of descending dopaminergic pathways. Previously, we reported the actions of dopamine (DA) on dorsal horn neurons as a descending inhibitory system based on in vivo whole-cell patch-clamp methods. However, some studies have recently demonstrated that DA facilitates pain in the neuropathic pain model. In the present study, we investigated the effect of DA on excitatory synaptic transmission in the dorsal horn of the rat spinal cord using whole-cell patch-clamp methods. In the neuropathic pain model rats, quinpirole, a D2-like receptor agonist, frequently produced inward currents compared to that in normal rats. Inward currents indicate that depolarization of the dorsal horn neurons lead the pain facilitation. These results suggest that DA-induced effects in the dorsal horn might modulate the descending inhibitory system to the descending facilitatory system in neuropathic pain.
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| Academic Significance and Societal Importance of the Research Achievements |
A11領域から脊髄後角に投射しているドーパミン作動神経系は本来生理的条件下では下行性疼痛抑制系を形成しているが、今回の研究成果から神経障害性疼痛時にはD2-like受容体の役割が本来の疼痛抑制を担う細胞の過分極から疼痛賦活になる細胞脱分極を形成するように何らかの変調を来している可能性があると考えられる。このことは神経障害性疼痛の状況下では、生理的に備わる下行性疼痛抑制を賦活する方法での疼痛コントロールが難しい側面を有していることを示唆している。
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