| Project/Area Number |
16K15197
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Environmental physiology(including physical medicine and nutritional physiology)
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| Research Institution | National Institute of Advanced Industrial Science and Technology |
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Principal Investigator |
SHICHIRI Mototada 国立研究開発法人産業技術総合研究所, バイオメディカル研究部門, 研究グループ長 (20434780)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | ストレス / 脂質酸化物 / 脳内モノアミン / 客観的評価指標 / 酵素 |
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| Outline of Final Research Achievements |
We had founded that 12-HETE, 12-lipoxygenase metabolite of arachidonic acid, specifically increased in mouse plasma after stress load. And, we also demonstrated that 12-HETE induces the escape behavior. However, 12-HETE did not increase in mouse brain tissue after stress load, the signal pathway by which 12-HETE increased in plasma transmits to the brain was unclear. In this study, we hypothesized that 12-HETE signal are transmitted to the brain via the 12-HETE receptor expressed in peripheral nerves. We found out that the inhibitor of 12-HETE receptor could suppress the escape behavior and 12-HETE is involved in stress-induced release of noradrenaline in brain tissue. These results suggested that 12-HETE is a novel stress pathway different from the already known pathway.
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