| Project/Area Number |
12670100
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Tokyo Metropolitan Institute of Gerontology |
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Principal Investigator |
OHTA Minoru Tokyo Metropolitan Institute of Gerontology, Assistnat researchoer of Dept. Clini. Physiol.Researcher, 臨床生理部門, 助手 (70133634)
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| Co-Investigator(Kenkyū-buntansha) |
MIYASAKA Kyoko Tokyo Metropolitan Institute of Gerontology, Assistnat researchoer of Dept. Clini. Physiol. Head, 臨床生理部門, 室長 (90166140)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2000: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | CCK / CCK-A receptor / CCK-B receptor / Gastric emptying / knokout mice / gene / gene expression / CCK-A受容体ノックアウトマウス / CCK-B受容体ノックアウトマウス / CCK-AB受容体ノックアウトマウス |
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| Research Abstract |
Cholecystokinin (CCK) is an important gastrointestinal hormone as well as neurotransmitter. Two types of CCK receptors (type A and type B) have been identified. The CCK-A receptor is known to be involved in satiety, food intake and behavior and the B receptor to be involved in anxiety. As we recently raised CCK-A, -B and AB receptor knockout mice, the role of these receptors was determined.
CCK-BR(-/-) and AR(-/-)BR(-/-) mice showed increased anxiety states compared with CCK-AR(+/+)BR(+/+) and AR(-/-) mice. Previous reports showed that panic attack and anxiety could be induced by CCK-4, which predominantly bound CCK-BR. Our observation was not compatible for the previous report. Further study is necessary.
The daily energy intake and energy expenditure were significantly higher in CCK BR(-/-) and CCK-AR(-/-)BR(-/-) mice than CCK-AR(-/-) and wild-type [CCKAR(+/+)BR(+/+)] mice. The ratios of liver and kidneys per body weight (g-kg) were significantly higher in CCKAR(-/-)BR(-/-) mice than wild-type mice. Energy metabolism and energy turnover were increased under the condition of disruption of CCK-BR gene, although the real mechanism is unknown.
Gastric emptying was not delayed in CCK-AR(-/-) mice. Gastric emptying was enhanced in CCK-BR(-/-) and AR(-/-)BR(-/-) mice. However, administration of atropine significantly inhibited gastric emptying in all mice. CCK-8 delayed gastric emptying in CCK-AR(+/+)BR(+/+) and BR(-/-) mice, but not in CCK-AR(-/-) and AR(-/-)BR(-/-) mice.
In mice, CCK, acetylcholine, and GRP could stimulate amylase release from the pancreas, whereas only CCK could induce gallb ladder contration.
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