| Project/Area Number |
15K09862
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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 |
Psychiatric science
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| Research Institution | University of Miyazaki (2017-2018)
Hamamatsu University School of Medicine (2015-2016) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
村上 元 埼玉医科大学, 医学部, 講師 (70613727)
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| Research Collaborator |
SUENAGA Toshiko
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| Project Period (FY) |
2015-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 主要組織適合遺伝子複合体 / 注意欠如・多動性障害 / 側坐核 / ドーパミン受容体 / メチルフェニデート / MHC-I / マウス / 社会的行動 / プレパルスインヒビション / 多動性 / 衝動性 / 注意機能 / 不注意 |
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| Outline of Final Research Achievements |
Mice deficient in the function of major histocompatibility complex antigen class I (MHC-I) showed a human attention deficit/hyperactivity disorder-like phenotype, such as hyperactivity, motor impulsiveness, and inattention. In addition, expression of nucleus accumbens dopamine 1 receptor (D1R) was increased in MHC-I deficient mice. Administration of methylphenidate, a treatment for ADHD, to these mice ameliorated all symptoms of hyperactivity, impulsiveness and attention disorders. Furthermore, c-Fos expression of neurons with D1R in nucleus accumbens was significantly suppressed by methylphenidate.
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| Academic Significance and Societal Importance of the Research Achievements |
MHC-I機能欠損マウスは、動物モデルとして、表面的妥当性、予測的妥当性、および構成的妥当性の３つの基準を概ね満たしており、長い間不明のままにあるADHDの病態メカニズムの解明に一歩近づくことが期待できる。
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