| Project/Area Number |
15591207
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | Hokkaido University |
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Principal Investigator |
ABEKAWA Tomohiro Hokkaido Universiry, Hokkaido University Hospital, Inst., 大学病院, 助手 (80301901)
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| Co-Investigator(Kenkyū-buntansha) |
KUSUMI Ichiro Hokkaido University, Hokkaido University Hospital, Lec., 大学病院, 講師 (30250426)
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| Project Period (FY) |
2003 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2005: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2004: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | schizophrenia / treatment-resistant / model for pathophysiology / prefrontal cortex / psychostimulant |
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| Research Abstract |
We can use an NMDA receptor dysfunction model for the treatment-resistant schizophrenia, and methamphetamine model for the treatment-responsive model for schizophrenia. We hypothesized that increased glutamate levels in the medial prefrontal cortex(mPFC) and the nucleus accumbens(NA) induced by high dose of methamphetamine play an important role for the development of behavioral cross-sensitization to an NMDA receptor antagonist. We have shown that a protein kinase C inhibitor, staurosporine and a GABA stimulant, valproate block the development of the cross-sensitization to dizocilpine. Valproate and olanzapine potently, and risperidone moderately inhibited high dose of methamphetamine-induced delayed increases in glutamate levels in the mPFC and the NA.
These findings suggest that valproate, olanzapine, and risperidone may block the development of the treatment-resistance of schizophrenia.
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