Study on the role of emotional stress on the pathogenesis of schizophrenia and mood disorder.---To clarify the relationship between emotional stress and central neural systems of monoamine and glutamate by using animal models of psychiatric disorders---
| Project/Area Number |
14570901
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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 |
INOUE Takeshi Hokkaido Univ., Hospital, Lec., 医学部・歯学部附属病院, 講師 (70250438)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2002: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | fear conditioning / c-Fos protein / mediodorsal nucleus of the thalamus / amygdala / selective serotonin reuptake inhibitor / serotonin / brain microinjection study / 中隔 |
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| Research Abstract |
The purpose of this study is to examine the functional role of various brain regions for anxiety and the relationship between glutamate/monoamine neurotransmission and emotional behavior.
1)Damages to the mediodorsal nucleus of the thalamus and the amygdale interfered with both the acquisition and expression of contextual fear conditioning. Septal lesions reduced only the expression of contextual fear conditioning.
2)Microinjection of a selective serotonin reuptake inhibitor (SSRI) into the basolateral nucleus of the amygdala reduces freezing behavior induced by conditioned fear.
3)Microinjection of NMDA receptor antagonists into the amygdale and mediodorsal nucleus of the thalamus reduces freezing behavior induced by conditioned fear.
4)Conditioned fear induced c-Fos expression in the amygdala and this increased c-Fos expression was attenuated by SSRI administration and extinction trials. Reduced c-Fos expression was accompanied by reduced freezing behavior as an index of fear. These results suggest that increased serotonin induced by SSRIs inhibits neuronal activities in the amygdala and reduces fear. This serotonin hypothesis may explain the mechanism of anxiolytic action of SSRIs.
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Report
(3 results)
Research Products
(37 results)
