| Project/Area Number |
26461727
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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 | Kindai University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
白川 治 近畿大学, 医学部, 教授 (40243307)
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| Research Collaborator |
TAMMINGA CA University of Texas Southwestern Medical Center, Professor
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 抗精神病薬 / 統合失調症 / Kv3ファミリー / Kv3.1 / Kv3.2 / GAD65 / GAD67 / 前頭葉 / パルブアルブミンニューロン / 定型抗精神病薬 / 非定型抗精神病薬 / 前頭前野 / Ｋｖ3.1 / Ｋｖ3.2 |
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| Outline of Final Research Achievements |
In this study, we found that haloperidol, a typical APD and risperidone, an atypical APD differentially modulated cortical Kv3.1 and Kv3.2 channels. While both haloperidol and risperidone significantly increased Kv3.1 protein levels in rat prefrontal cortex, Kv3.2 protein levels showed an increase and a decrease in the same region by haloperidol and risperidone, respectively. A similar pattern of Kv3.2 change was found in cerebellum, however, no significant changes were found in Kv3.2 protein levels in hippocampus, thalamus and striatum. These result were reported in Annual Meeting of the Japanese Society of Psychiatry and Neurology.
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