| Project/Area Number |
15K14348
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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 | Niigata University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
NAMBA Hisaaki 新潟大学, 脳研究所, 助教 (90332650)
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| Research Collaborator |
SAITO Mami 新潟大学, 大学院医歯学総合研究科
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | サリドマイド / レナリドミド / セレブロン / ユビキチン / セロトニン神経 / セロトニン / 神経発火 / フタルイミド化合物 / ドパミン / プロテアソーム |
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| Outline of Final Research Achievements |
Thalidomide was sold in Japan as gastrointestinal drugs and sleeping pills, but it was considered teratogenic and was forbidden to use in September 1962. Professor Honda et al., 2010, revealed that thalidomide binds to the cerebron molecule constituting the ubiquitin ligase complex to inhibit ubiquitination. However, the hypnotic and sedative effects of thalidomide can not be mimicked by a cereblon ligand, lenalidomide. We attempted to elucidate the central action of this drug. Using various types of mouse brain slice preparations, we electrophysiologically assessed the pharmacological actions of the thalidomide derivatives or an ubiquitin-proteasome inhibitor and found that the central actions of thalidomide cannot be illustrated by its binding to cereblon.
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