receptors in pathology of epilepsy induced by kainic acid
| Project/Area Number |
15K07970
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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 |
Pharmacology in pharmacy
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| Research Institution | Hokuriku University (2016-2017)
Kitasato University (2015) |
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Principal Investigator |
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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 |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | てんかん / プロスタグランジンE2 / EP3受容体 / カイニン酸 / 神経炎症 / 痙攣 / 神経細胞死 / ミクログリア / 癲癇 / 炎症 / 不安 / ノックアウトマウス |
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| Outline of Final Research Achievements |
The expression of COX-2, mPGES-1 and EP3 receptors were increased in hippocampus of kainic acid (KA)-induced seizure mice. The seizure score and hippocampal neurotoxicity in EP3 knockout (KO) mice was significantly lower than that in wild-type (WT) mice. The glial activation and inflammatory responses after seizures were also less severe in EP3KO mice as compared with WT mice. These results suggest that activation of EP3 receptors after KA injection contributes to seizure susceptibility, glial activation and hippocampal neuronal loss. Thus, inhibition of EP3 receptors will be a valuable therapeutic option in treatment of temporal lobe epilepsy.
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Report
(4 results)
Research Products
(13 results)
