Elucidatoin of physiological role of muscarinic receptors in the adrenal medullary cell by using muscarinic receptor deficient mouse
Project/Area Number |
25460306
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General physiology
|
Research Institution | University of Occupational and Environmental Health, Japan |
Principal Investigator |
HARADA Keita 産業医科大学, 医学部, 助教 (50399200)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
Keywords | ムスカリン受容体 / ノックアウトマウス / 低血糖 / カテコールアミン / 副腎髄質細胞 / TRPCチャネル / 血糖値 / インスリン / アドレナリン |
Outline of Final Research Achievements |
We have examined that the role of muscarinic receptors on the catecholamine secretion of adrenal medullae during hypoglycemia by using muscarinic receptors-deficient mice (KO mouse). After fasting for 24h, insulin was dosed in KO and wild-type (WT) mice and the amount of catecholamine in the plasma of both mice was compared. There was no significant difference between the catecholeamine amount in the plasma of KO mice and that of WT mice. On the other hand, it was found that non-selective cation channels (TRPC channels) together with STIM1 molecule were involved in the catecholamine secretion on the muscarinic stimulation in guinea-pig adrenal medullary (AM) cells. We have also demonstrated that TRPC channels were translocated from cytoplasm to cell periphery in response to muscarine in guinea-pig AM cells and PC12 cells.
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Report
(4 results)
Research Products
(7 results)