| Project/Area Number |
26290029
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Laboratory animal science
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| Research Institution | Niigata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
藤澤 信義 新潟大学, 脳研究所, 助教 (50199311)
前田 宜俊 新潟大学, 脳研究所, 助教 (00754524)
小田 佳奈子 新潟大学, 脳研究所, 助教 (60708212)
佐藤 俊哉 北里大学, 医学部, 教授 (90359703)
大久保 直 北里大学, 医学部, 准教授 (10450719)
佐藤 朝子 北里大学, 医学部, 臨時職員(研究職) (10465932)
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| Research Collaborator |
NAKAO Satohiro
NAMBU Atsushi
CHIKEN Satomi
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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 |
¥16,900,000 (Direct Cost: ¥13,000,000、Indirect Cost: ¥3,900,000)
Fiscal Year 2016: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2015: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2014: ¥7,280,000 (Direct Cost: ¥5,600,000、Indirect Cost: ¥1,680,000)
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| Keywords | D1ドーパミン受容体 / D2ドーパミン受容体 / 運動制御 / 大脳基底核回路 / パーキンソン病 / 遺伝子操作マウス / テトラサイクリン制御システム / 神経活動 / ドーパミン受容体 / 可逆的発現制御マウス / 電気生理学的解析 / 学習記憶 / 運動学習 / 運動調節 / 時期特異的発現抑制 / 電気生理学的性質 / 発達期 / パーキンソン病モデル動物 / 遺伝子改変マウス / 時期特異的ノックダウン / 生殖工学的技術 / ニホンザル / 運動機能調節 |
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| Outline of Final Research Achievements |
Using genetically modified mice that reversibly suppress expression of dopamine D1 receptor (D1R) by drug (doxycycline) administration, D1R deficiency leads to decrease of motor activity. Normally, the electrical stimulation at motor cortex travels through three pathways (hyper-direct, direct and indirect pathways) and is recorded as neural activity of triphasic "excitation - suppression - excitement" in the entopeduncular nucleus, the output part of the basal ganglia. In the state of D1R deficiency, 'suppression' disappeared. It is believed that this "suppression" passes through the direct pathway of the basal ganglia circuit and works for induction of movement. In this study, information via D1R is thought to be indispensable for signaling of the direct pathway and induction of movement, and a decrease in the dynamic transmission of signals through the direct pathway is thought to lead to motor symptoms of Parkinson's disease.
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