| Project/Area Number |
15K06776
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
Ibi Masakazu 京都府立医科大学, 医学(系)研究科(研究院), 講師 (10336539)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | NADPHオキシダーゼ / 活性酸素種 / 末梢神経障害 / 不安様行動 / うつ様行動 / 難治性疼痛 / いたみ |
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| Outline of Final Research Achievements |
Development of the tactile allodynia was demonstrated until 4 weeks after SNI. Administration of paclitaxel and oxaliplatin induced allodynia, which sustained for 7 days, while bortezomib-induced allodynia sustained for 4 weeks. There was, however, no difference in the levels of neuropathic pain between WT and Nox1-KO. On the other hand, the SNI-induced anxiety- and depressive-like behaviors were significantly suppressed in Nox1-KO. In the hippocampus and hypothalamus of WT, the expression of NOX1 mRNA was significantly elevated following SNI. Delivery of miRNA against NOX1 to the hippocampus, but not to the hypothalamus of WT, restored SNI-induced emotional behaviors without affecting mechanical allodynia.
Taken together, the anxiety- and depressive-like behaviors induced by neuropathic pain may be mediated by up-regulation of NOX1 in the hippocampus.
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