| Project/Area Number |
16K19749
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Psychiatric science
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| Research Institution | Chiba University |
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Principal Investigator |
Oda Yasunori 千葉大学, 大学院医学研究院, 助教 (50770583)
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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 |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | DSP / DRD2 / GSK3 / glutamate / NMDA receptor / グルタミン酸 / NMDA受容体 / ES / ドパミン過感受性精神病 / ドパミンD2受容体 / グリコーゲン合成酵素 / γ-アミノ酪酸 / N-メチル-D-アスパラギン酸受容体 / 統合失調症 / グリコーゲン合成酵素3 / リチウム |
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| Outline of Final Research Achievements |
Western blot analysis revealed significant reduction in Striatal GSK-3α/β in DSP model rats compared with that in non DSP and controls, while there were no statistically significant difference in AKT, pGSK-3β.
On the other hand, glutamatergic signaling is relatively decreased to GABA in DSP rats. Our results also showed that excessive doses of haloperidol can induce striatal NMDAR hypofunction in non-DSP rats, which could prevent the formation of tardive dyskinesia but cause treatment resistance. In view of the need for therapeutic strategies for treatment-resistant schizophrenia, further research exploring our present findings is necessary.
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