| Project/Area Number |
22591269
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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 | National Center of Neurology and Psychiatry |
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Principal Investigator |
HATTORI Kotaro 独立行政法人国立精神・神経医療研究センター, 神経研究所 疾病研究第3部, 室長 (50415569)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 神経科学 / 精神疾患 / 薬理学 / シグナル伝達 / 統合失調症 / 抗精神病薬 / Fynキナーゼ / D2受容体 / NMDA受容体 |
|---|
| Research Abstract |
We have identified two molecules as downstream substrates for Fyn-mediate anti-psychotic signaling. For one of those molecules, we also determined antipsychotics-mediate phosphorylation sites. Using post-mortem brain samples, we found that the Fyn protein levels are increased in the schizophrenia frontal cortices compared to the controls. Also, the mRNA expression of CADPS2, which is involved in the exocytosis of monoamines, was increased in schizophrenia brains. In the cerebrospinal fluids, the levels of IL-6, which is upstream regulator of Fyn, and the levels of dopamine metabolite, HVA, were increased in schizophrenia. Thus, we have identified a group of molecules involved in antipsychotic signaling and, found that a part of those molecules should be involved in the schizophrenia pathology. Further research is required to clarify whether those molecules could be therapeutic targets for schizophrenia.
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