| Project/Area Number |
15K09846
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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 |
Psychiatric science
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| Research Institution | Kawasaki Medical School |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
陸 豊 川崎医科大学, 医学部, 助教 (20708557)
岡部 直彦 川崎医科大学, 医学部, 助教 (30614276)
氷見 直之 川崎医科大学, 医学部, 講師 (70412161)
宮崎 哲治 川崎医科大学, 医学部, 助教 (50412185)
丸山 恵美 川崎医科大学, 医学部, 助教 (30792072)
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| Research Collaborator |
NARITA Kazuhiko
SHIROMOTO Takashi
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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 | 電気けいれん療法 / ストレス / うつ様モデル / カルシウムシグナル系 / リアノジン受容体 / イノシトール三リン酸受容体 / マウス / ECS / Ca2+ / ECT / うつ病 / 海馬 |
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| Outline of Final Research Achievements |
We have investigated it using mouse depression model focusing on intracellular Ca2+ signaling system in the hippocampus. The model were made by chronic stress (water immersion with restriction) and electroconvulsive shock (ECS) was given once a day for 2 weeks after completion of depression. Depression like behaviors such as forced swimming test (FST) and novelty suppression feeding test (NSF) were observed in the model mice, and ECS improved these abnormalities. Both inositol trisphosphate receptor (IP3R) and ryanodine receptors (RyRs) which were Ca2+ modulating factors were increased by chronic stress, while CaMK were not changed. Furthermore, dantrolene which is RyRs antagonist inhibited the effects of ECS in both FST and NSF. These results suggest that the upregulation of Ca2+ signaling system might be occurred by the stress induced suppression in neuronal activity of the hippocampus and ECT might activate it by the increase of intracellular Ca2+.
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