| Project/Area Number |
23790599
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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 |
Applied pharmacology
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| Research Institution | Osaka University |
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Principal Investigator |
AGO Yukio 大阪大学, 大学院・薬学研究科, 助教 (50403027)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | うつ病 / 代謝型グルタミン酸2/3受容体 (mGlu2/3受容体) / 環境要因 / グルココルチコイド / グリア細胞 / 大脳皮質前頭前野 / 海馬 / ドパミン / 代謝型グルタミン酸2/3受容体 / 環境ストレス / グルタミン酸神経系 |
|---|
| Research Abstract |
Only 30-50% of patients with depression enter remission after antidepressant treatment. Thus, discovering novel neuronal mechanisms of pathophysiology of depression as well as more effective treatments are necessary. In this study, metabotropic glutamate 2/3 receptor antagonists showed antidepressant-like effects in chronic glucocorticoid-treated mice, an animal model of conventional antidepressant-resistant depression. Chronic glucocorticoid treatment markedly increased prefrontal dopaminergic activity, and this enhanced activity was blocked by metabotropic glutamate 2/3 receptor antagonists, but not conventional antidepressants. The present findings suggest that the metabotropic glutamate 2/3 receptor is a promising target for the treatment of patients with treatment-resistant depression.
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