2005 Fiscal Year Final Research Report Summary
Study of model for pathophysiology and mechanism for the treatment of the treatment resistant schizophrenia
| 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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| 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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[Book] 覚醒剤精神病と麻薬依存2004
Author(s)
小山司, 安部川智浩, 本田稔, 伊藤耕一
Total Pages
68-78
Publisher
逆耐性現象と興奮性アミノ酸神経伝達
Description
「研究成果報告書概要(和文)」より
