The role of AMPA receptor GluR1 for rapid-acting antidepressant behavior
Project/Area Number |
26860481
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
General internal medicine(including psychosomatic medicine)
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Research Institution | Yamaguchi University |
Principal Investigator |
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Project Period (FY) |
2014-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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Keywords | CaMKIIβ / ストレス / うつ病 / 抗うつ作用 / GluR1 / 抗うつ効果 / depression |
Outline of Final Research Achievements |
aThe aim of this study is to elucidate the molecular mechanism underlying HDAC inhibitor SAHA-induced rapid-acting antidepressant behavior. We found that SAHA increases mRNA expression of CaMKIIβ, which in turn enhances the phosphorylation of AMPA receptor GluR1, resulting in increased trafficking of GluR1 in synaptic membrane in the hippocampus of mice treated with SAHA. Together, these results suggest CaMKIIβ-GluR1 signaling might be associated with SAHA-induced rapid-acting antidepressant behavior.
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Report
(3 results)
Research Products
(1 results)