| Project/Area Number |
22700384
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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 |
Nerve anatomy/Neuropathology
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| Research Institution | National Research Institute for Child Health and Development |
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Principal Investigator |
NAKAMURA Kazuaki 独立行政法人国立成育医療研究センター, 研究所薬剤治療研究部, 室長 (80392356)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | バソプレッシン / 神経細胞保護 / 海馬 / バソプレッシン受容体 / グリア細胞 |
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| Research Abstract |
In this study, the roles of vasopressin(AVP) for neural cell death were examined. The gene expression analysis and innmunohistochemical analysis revealed that V1a receptor and V1b receptor were expressed in hippocampal neuron and astrocyte, and that AVP was expressed in hippocampal astrocyte. AVP could reduce the kainic-acid induced hippocampal neural death in vitro. Kainic-acid induced hippocampus degeneration model showed that seizure severity of V1a receptor and V1b receptor knock out mice were reduced compare to wild type mice, respectively. These results suggest that AVP could protect hippocampal neuron via V1a and/or V1b receptor, and that AVP could protect hippocampal neuron via astrocyte indirectly as well as to neuron directly. On the other hand, immunohistochemical analysis for neural degeneration in kainic-acid induced hippocampus degeneration model showed that kainic-induced neural degeneration was more severe in V1a receptor knock out mice than in V1b receptor knock out mice. This result suggests that there are difference of neural protective function between V1a receptor and V1b receptor. Thus, it is suggest that investigation of AVP function for glial function as well as neural function lead to novel therapy strategy for neural degeneration disease using AVP and/or AVP agonist/antagonist.
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