| Project/Area Number |
21790376
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Experimental pathology
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| Research Institution | The University of Tokushima (2010)
Tohoku University (2009) |
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Principal Investigator |
KASAHARA Jiro The University of Tokushima, 大学院・ヘルスバイオサイエンス研究部, 准教授 (10295131)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2009: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | うっ病モデル / 神経新生 / 抗うつ薬 / セロトニン / 可塑性 / うつ病 / 疾患モデル動物 / ストレス / カルシウムシグナル / 神経再生 |
|---|
| Research Abstract |
CaMKIV is a calcium/calmodulin-dependent protein kinase which is found abundantly in the nuclei of central neurons, and CaMKIV knock out mice showed attenuated sensitivity to antidepressants. I examined sensitivity to early life stress of this mice using maternal separation paradigm. In wild type C57BL/6 mice, some of the depression-and anxiety-related behaviors were deteriorated by the early life stress. In CaMKIV knock out mice with the early life stress, similar or even worse results were obtained in the same behavioral analysis. I also examined serotonin-induced CaMKIV activation using cultured cortical neurons of mice. Serotonin activated CaMKIV and MAPK/ERK, concomitant with increase of the phosphorylation of a transcriptional factor CREB, suggesting this mechanism is required for the effect of antidepressants and regulation of mood.
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