The neurobiological basis of anxiety disorder focusing on emotional regulation
| Project/Area Number |
25861027
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Psychiatric science
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| Research Institution | Health Sciences University of Hokkaido |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 社交性不安障害 / 神経科学 / 内側前頭前野 / セロトニン / 5-HT1A受容体 / 行動薬理学 / 電気生理学 / 精神医学 / 神経薬理学 / 不安障害 |
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| Outline of Final Research Achievements |
In the present study, we attempted to determine the neurobiological basis of anxiety disorder. First, we revealed that chronic social defeat stress impaired social anxiety of mice. Moreover, serotonin 5-HT1A receptor agonist, 8-OH DPAT, did not produce anxiolytic action in social defeated mice. However, chronic administration of serotonin reuptake inhibitor, fluoxetine, improved social anxiety induced by chronic social defeat stress. In the electrophysiological experiments, pyramidal cells in layer V of the medial prefrontal cortex (mPFC) did not show the hyperpolarization elicited by 5-HT1A receptor stimulation, indicating that chronic social defeat stress induced 5-HT1A receptor dysfunction in the mPFC. In future experiment, we need to reveal which the change pattern of 5-HT1A receptor dysfunction is quantitative and/or qualitative dysfunction.
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Report
(3 results)
Research Products
(10 results)
