| Project/Area Number |
16K14580
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | Osaka Yukioka College of Health Science |
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Principal Investigator |
SHIOSAKA SADAO 大阪行岡医療大学, 医療学部, 教授 (90127233)
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| Co-Investigator(Kenkyū-buntansha) |
吉田 成孝 旭川医科大学, 医学部, 教授 (20230740)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | KLK8 / ニューロプシン / ニューレグリン１ / ErbB4 / シナプス形成 / シナプトパチー / カリクレインペプチダーゼ / ErvB4 / Neuregurin1 / パルブアルブミン / γ帯域脳波 / 認知症 / 統合失調症 / 双極障害 |
|---|
| Outline of Final Research Achievements |
Social mammals recognize and discriminate their conspecifics to make pair bonding, to maintain species, to create social hierarchy, and to live in the society to which they belong. We investigated whether kallikrein 8 (KLK8)-neuregulin1-ErbB4 signaling is crucial for the social behavior. Using social discrimination paradigm of a three chamber behavioral task, we found neuregulin1-deactivated mouse (klk8-knockout mouse) impaired social discrimination, while this mouse exhibited normal social approach. Intraventricular injection of NRG1 177-246 (active domain of neuregulin1) into the brain of klk8-knockout mouse recovered the impairment into the level of wild type mouse and thus, KLK8 is one of the key regulator through NRG1-ErbB4 signaling, and contributes to social discrimination behavior.
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