| Project/Area Number |
10670916
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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 | University of The Air |
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Principal Investigator |
SEMBA Junichi UNIVERSITY OF THE AIR, ASSOSIATE PROFESSOR, 教養学部, 助教授 (30183429)
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| Co-Investigator(Kenkyū-buntansha) |
SUHARA Testuya NATIONAL INSTITUTE RADIOLOGICAL SCIENCE, CHIEF RESEARCHER, 高度診断研究ステーション, 主任研究官 (90216490)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | NEURODEVELOPMENTAL ABNORMALITY / SCHIZOPHRENIA / ANIMAL MODEL / 神経発達障害仮説 / 一酸化窒素 / ドーパミンD1受容体 |
|---|
| Research Abstract |
In order to clarify the neurobiological basis for neurodevelopmental hypothesis of schizophrenia, we tried to develop an animal model of schizophrenia by means of prenatal treatments with some psychoactive substances. Neonatal treatment with nitric oxde synthase inhibitor, L-NAME, resulted in decreased behavioural activity induced by methamphetamine. Neonatal treatment with dopamine D1 antagonist SCH23396, however, had no effect. Both treatments did not affect the development of sensitisation induced by methamphetamine. Chronic treatment with phencyclidine during neonatal period reduced melhamphetamine-induced behavioural stereotypy. This behavioural manifestation was also confirmed by c-fos mRNA expression induced by methamphetamine. These results suggest that, a certain neonatal pharmacological treatment may mediate hypofunction of dopamine in the brain as revealed by either behaviourally or neurochemically.
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