| Project/Area Number |
21790224
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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 |
Environmental physiology (including Physical medicine and Nutritional physiology)
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| Research Institution | Shinshu University |
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Principal Investigator |
MASUKI Shizue Shinshu University, 大学院・医学系研究科, 助教 (70422699)
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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 |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | 自発運動 / vasopressin V1a受容体 / 血圧反射 / 脳波 / 脳血流 / 運動 |
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| Research Abstract |
[Control study] We continuously measured cerebral activity and baroreflex control of HR in freely moving control mice. We found that cerebral activation suppressed baroreflex control of heart rate (HR) in their daily life, and after these sequential responses, mice started to move at 5 times higher probability than after a given time, suggesting tight linkages between cerebral activity, baroreflex control of HR, and voluntary locomotion. [V1a knockout study] We assessed any role of vasopressin V1a receptor in these sequential responses. We continuously measured the variables mentioned above in V1a receptor knockout (KO) and wild-type mice (WT). We found that suppression of baroreflex control of HR in response to voluntary activation of the cerebral cortex was abolished in KO mice. Moreover, the probability that mice started to move after cerebral activation was markedly lower in KO than WT mice with less suppression of baroreflex control of HR. These results suggest that V1a receptor plays an important role in starting voluntary locomotion after cerebral activation through suppression of baroreflex control of HR.
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