Molecular mechanism of nerve regeneration and sensory disorder following axonal injury
| Project/Area Number |
15K11057
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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 |
Functional basic dentistry
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| Research Institution | Nihon University |
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Principal Investigator |
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| Project Period (FY) |
2015-10-21 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 軸索損傷 / 神経回路 / 下歯槽神経 / 三叉神経脊髄路核 / ERK / 神経損傷 / 細胞接着分子 / CGRP / IB4 |
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| Outline of Final Research Achievements |
To study each process of anatomical, neurochemical and physiological regeneration after nerve injury, we developed a model of complete IAN transection (IANX) in mice. A subset of small TG neurons, i.e. C afferents, had re-innervated their appropriate receptive field within 2 weeks post-axotomy, and the peptidergic neurons regenerate more efficiently compared to non-peptidergic neurons after trigeminal nerve injury. On the other hand, head-withdrawal threshold (HWT) to noxious heat or pinch stimulation began to return toward basal level on day 14 after IANX, but did not recover completely. The distribution pattern of pinch stimuli-induced pERK-IR cells, i.e. second order neurons and/or interneurons, was altered in Vc at 2 weeks after IANX. We also found that the reduction in E-cadherin expression in Vc is correlated with increase of HWT to noxious stimuli after IANX.
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Report
(4 results)
Research Products
(7 results)
