| Project/Area Number |
18K15500
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 52030:Psychiatry-related
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| Research Institution | Kawasaki Medical School |
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Principal Investigator |
Maruyama Emi 川崎医科大学, 医学部, 助教 (30792072)
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| Project Period (FY) |
2018-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | うつ / 電気けいれん療法 / リアノジン受容体 / Ca2+ / 海馬 / RyRs / ECS / ダントロレン / IP3受容体 |
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| Outline of Final Research Achievements |
This study examined changes in the expression and function of ryanodine receptors (RyRs) and IP3 receptor (IP3R) in the central nervous system of a depression-like model mice, with the aim of demonstrating that RyRs may be a new target for antidepressant drugs. RyRs protein expression was significantly increased in the hippocampus and decreased with improvement of depressive-like symptoms induced by electroconvulsive shock (ECS), while no significant changes were observed in IP3R. RyRs antagonists exacerbated depressive-like symptoms and attenuated the antidepressant effect of ECS. Ca2+ release via RyRs was also decreased during depressive-like symptoms, but was restored by ECS. These results suggest that the Ca2+ release function of RyRs is involved in the onset and improvement of depression.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究はうつ病に最も有効な治療の一つである電気けいれん療法（ECT）の作用機序を調べることで薬物療法（抗うつ薬）への転換を図るものである。現行の抗うつ薬の有効性はさほど高くなく、ECTは処置病院にある程度の規模を要する。よって有効性の高い抗うつ薬に転換できればより多くの治療が可能となる。今回うつ状態で海馬のリアノジン受容体に変化が見られたことから中枢神経系におけるリアノジン受容体の機能回復が新薬の標的となり得る可能性を示した。
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