| Project/Area Number |
15K15031
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
General physiology
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| Research Institution | Okayama University |
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Principal Investigator |
Matsui Hideki 岡山大学, 医歯薬学総合研究科, 教授 (30157234)
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| Co-Investigator(Kenkyū-buntansha) |
松下 博昭 岡山大学, 医歯薬学総合研究科, 助教 (60732394)
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| Research Collaborator |
Hein Min Latt
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | オキシトシン / 絆 / ストレス / 社会行動 / コルチコステロン |
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| Outline of Final Research Achievements |
Oxytocin (OT), a neuropeptide produced from the paraventricular nucleus and the supraoptic nucleus of the hypothalamus, involves in maternal and social behaviors and male-female pair bonding. OT has been shown to mediate antistress and antidepressant-like effects in mice and rats. Glucocorticoids, corticosterone (CORT) in rodents, are released from adrenal cortex in response to stressful stimuli. Their overexposure in animals has been implicated in dendritic atrophy, apoptosis of hippocampal neurons and hippocampal dysfunction. We found that CORT induced the dendritic atrophy as well as apoptosis in primary cultures of mouse hippocampal neurons, both of which were prevented by co-treatment with OT. We also found that plasma CORT levels were lower in mating male mice compared to non-mating counterparts, and this effect was lost in OTR-KO mice. The findings suggest that there might be interplay between OT and glucocorticoids in stress regulation.
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