Project/Area Number |
16K10984
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Anesthesiology
|
Research Institution | Kyoto Prefectural University of Medicine |
Principal Investigator |
Shibasaki Masayuki 京都府立医科大学, 医学(系)研究科(研究院), 講師 (20405319)
|
Co-Investigator(Kenkyū-buntansha) |
天谷 文昌 京都府立医科大学, 医学(系)研究科(研究院), 教授 (60347466)
|
Project Period (FY) |
2016-04-01 – 2020-03-31
|
Project Status |
Completed (Fiscal Year 2019)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 神経障害性疼痛 / マイクログリア / M1型単球系細胞 / M2型単球系細胞 / 脾臓 / 脾臓由来単球系細胞 / 脳・神経 |
Outline of Final Research Achievements |
SNI model with splenectomy was used to investigate whether splenic monocytes was involved with mechanisms of neuropathic pain. Mechanical threshold was significantly decreased from day 1 after SNI or SNI with splenectomy procedure. Decreased mechanical threshold was observed in both ipsilateral and contralateral side. Mechanical threshold in the contralateral side of SNI with splenectomy was significantly decreased compared with solely SNI. Immunohistochemical analysis revealed that enhancement of signals of monocytic lineages was observed in the area of the spinal cord consistent with nerve injury. Areas of CD11b signal in the ipsilateral side on day 7 after SNI with splenectomy were significantly decreased.
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Academic Significance and Societal Importance of the Research Achievements |
これまで神経障害性疼痛発症のメカニズム解明には傷害側に焦点を当てた研究が主流であった。また神経損傷部位に一致した脊髄でのマイクログリア集積が知られているが、骨髄由来単球系細胞が神経損傷後に脊髄に浸潤すると報告がある。単球系細胞は脾臓にも存在するため、本研究では神経障害性疼痛モデルに脾臓摘出術を加えることで、神経損傷後に脊髄に集積する単球系細胞が脾臓由来かどうかを調査した。また脾臓摘出術を加えることで非傷害側の痛覚閾値が低下することがわかり、神経損傷後に脊髄に集積する単球系細胞が脾臓由来であり、かつそれらが脊髄内での何らかの影響を及ぼし、非傷害側の痛覚閾値の低下を引き起こしていることがわかった。
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