| Project/Area Number |
26460317
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Environmental physiology(including physical medicine and nutritional physiology)
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| Research Institution | Takasaki University of Health and Welfare |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
鯉淵 典之 群馬大学, 大学院医学系研究科, 教授 (80234681)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 育児行動 / 脳内環境 / 胎児期環境 / ドパミン-プロラクチン シグナル / CIN85 / ネグレクト / Nurturing behavior / 育児放棄 / プロラクチン |
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| Outline of Final Research Achievements |
CIN85 is involved in the regulation of receptor endocytosis. Mice deficient of CIN85 expression show maternal neglect. When wildtype (WT) embryos were transplanted into the fallopian tubes of CIN85 knockout (KO) mice, they also demonstrated inhibited nurturing behavior as adults. Conversely, when KO embryos were transplanted into the fallopian tubes of WT mice, the resultant pups exhibited normal nurturing behaviors. We detected decreased prolactin (PRL) levels in KO compared to WT mice. PRL injection in KO mice during pregnancy could partially rescue the defect in maternal behavior of the next generation. This correlates with our findings that neural circuitry associated with nurturing behaviors was less active in pups born to KO mothers, but PRL administration to mothers restored neural activity to normal levels. Our findings indicate an important role of CIN85 in the regulation of the PRL system in the brain and provide new insight into a molecular explanation for maternal behavior.
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