| 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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| 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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