Studies on the interoception and autonomic neurons based on the molecular pathophysiology of congenital insensitivity to pain with anhidrosis
| Project/Area Number |
21600010
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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 |
疼痛学
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| Research Institution | Kumamoto University |
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Principal Investigator |
INDO Yasuhiro 熊本大学, 医学部附属病院, 講師 (40244131)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 先天性無痛症 / 先天性無痛無汗症 / 遺伝性感覚自律神経性ニューパチーIV型 / 神経成長因子 / 神経成長因子受容体 / TRKA / NTRK1 / 内感覚 / NTRK |
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| Research Abstract |
Congenital insensitivity to pain with anhidrosis(CIPA) is a genetic disorder due to loss-of-function mutations in the NTRK1(TRKA) gene encoding TrkA, a receptor tyrosine kinase for NGF. Patients with CIPA lack NGF-dependent neurons, including polymodal receptors and sympathetic postganglionic neurons. Polymodal receptors play essential roles in interoception and report the physiological status of various tissues in the body to the brain. In response to interoception, the brain maintains homeostasis in the body via various neural mechanisms. Sympathetic neurons are indispensable for these mechanisms. Molecular pathophysiology of CIPA indicates that NGF-dependent neurons are essential for the establishment of neural networks for interoception and homeostasis, playing crucial roles in the brain-body interactions.
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Report
(4 results)
Research Products
(16 results)
