| Project/Area Number |
23590729
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pain science
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| Research Institution | Kinki University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SEKIGUCHI Fumiko 近畿大学, 薬学部, 准教授 (90271410)
TSUBOTA Maho 近畿大学, 薬学部, 助教 (90510123)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | カルシウムチャネル / ＰＫＡ / カルシニューリン / 痛み / 神経突起伸長 / 薬理学 / PKA / 神経突起 / イオンチャネル / カルシウム / プロテインキナーゼA / 疼痛制御 |
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| Research Abstract |
Among three isoforms of T-type calcium channels, Cav3.2 expressed abundantly in the peripheral ending of nociceptors plays a critical role in nociceptive processing. We thus examined molecular mechanisms for functional regulation of Cav3.2 by phosphorylation and dephosphorylation, and its impact on pain signals. Our data show that PKA, activated by stimulation of prostaglandin EP4 receptors in an AKAP150-dependent manner, phosphorylates and functionally upregulates Cav3.2, leading to hyperalgesia, and that calcineurin, a phosphatase, negatively regulates Cav3.2 functions.
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