2013 Fiscal Year Final Research Report
Identification of the control factor of occurrence and prolonged pain of scarring Identification of regulator generation and prolonged pain of scar
| Project/Area Number |
23590725
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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 | Aichi Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NISHIHARA Makoto 愛知医科大学, 医学部, 准教授 (60380325)
INOUE Shinsuke 愛知医科大学, 医学部, 講師 (80403905)
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| Research Collaborator |
KAJITA Yukihiro 愛知医科大学
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| Project Period (FY) |
2011 – 2013
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| Keywords | 瘢痕 / 慢性疼痛 / マクロファージ / コラーゲン線維 / CGRP / ED-1 / α-SMA |
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| Research Abstract |
The animal model with painful scar was developed in rats and mouse by extensively stripping subcutaneous tissue from the plantar in the hind paw. The mechanical pain threshold decreased specifically in the ipsilateral plantar in animals with scar. This state was maintained for 12 weeks. A collagen layer developed from fibers derma to the muscular layer in the scar tissue in which many fibroblasts were observed. No statistical differences were found for the areas of the c-Fos-immunoreactive (c-Fos-IR) neurons in the ipsilateral and contralateral sides of the L5 level of the dorsal horn in both the Scar group and Pinhole (sham operation) group. However, myelin sheath fragmentation of the nerve fibers was observed in the ipsilateral dorsal root at the L5 position. Similar behavioral findings were observed in mouse models and TNF and Interleukin associate mRNA was increased in ipsilateral DRG.
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