Drug discovery and neurochemical researches about T-type calcium channel in neurogenesis.
| Project/Area Number |
17K15456
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pharmacology in pharmacy
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Research Collaborator |
Xu Jing
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | T 型カルシウムチャネル / 神経新生 / 海馬神経新生 / 神経薬理学 / うつ様行動 / 薬理学 / 生理学 / 脳・神経、脳神経疾患 |
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| Outline of Final Research Achievements |
Number of depressive patients is over million in Japan, and it is serious social problem that depressive patients may account for 60% of suicides. We succeeded to develop T-type calcium channel enhancer. This compound improved depressive-like behaviors in olfactory-bulbectomized (OBX) mice. Whereas depressive-like behaviors are closely associated with hippocampal adult neurogenesis, T-type calcium channel enhancer could restore impaired hippocampal neurogenesis in OBX mice. In addition, T-type calcium channel enhancer enhanced monoamine releases in the mouse hippocampus, which have important role in depression. Finally, we observed impaired neurogenesis in the T-type calcium channel gene knock out mouse hippocampus. Taken together, we suggest that T-type calcium channel may have an important role in adult neurogenesis and brain homeostasis.
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| Academic Significance and Societal Importance of the Research Achievements |
既存の抗うつ薬はモノアミントランスポーターを阻害し、セロトニンやノルアドレナリンなどのモノアミンを増加させることで抗うつ効果を示す。しかしながら、抗うつ効果が得られるまでに時間がかかること、治療抵抗性うつ病患者の増加していることから新規作用機序の治療薬開発が求められている。また、T 型カルシウムチャネル賦活化薬の開発は世界初であり、研究のオリジナル性および独創性は極めて高いと考えられる。さらに、T 型カルシウムチャネルの脳高次機能については未だ不明な点が多く、神経新生やうつ病との関連が明らかになれば神経科学の発展と新規抗うつ薬の開発に大きく貢献できると考えられる。
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Report
(3 results)
Research Products
(8 results)
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[Journal Article] The Disease-modifying Drug Candidate, SAK3 Improves Cognitive Impairment and Inhibits Amyloid beta Deposition in App Knock-in Mice.2018
Author(s)
Izumi H, Shinoda Y, Saito T, Saido TC, Sato K, Yabuki Y, Matsumoto Y, Kanemitsu Y, Tomioka Y, Abolhassani N, Nakabeppu Y, Fukunaga K.
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Journal Title
Neuroscience.
Volume: 377
Pages: 87-97
DOI
Related Report
Peer Reviewed
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