2010 Fiscal Year Final Research Report
The elucidation of the reconstruction mechanism of the nucleus tractus spinalis sensory nerve in region of face cancer pain and the neuropathic pain
| Project/Area Number |
20592377
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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 |
Surgical dentistry
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| Research Institution | Kyushu Dental College |
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Principal Investigator |
NAKANISHI Osamu Kyushu Dental College, 歯学部, 教授 (50137345)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIKAWA Toshizo 山口大学, 医学部, 教授 (90034991)
HARANO Nozomu 九州歯科大学, 歯学部, 助教 (50423976)
KAI Aya 九州歯科大学, 歯学部, 助教 (80453231)
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| Co-Investigator(Renkei-kenkyūsha) |
YOSHIDA Mitsuhiro 九州歯科大学, 歯学部, 助教 (40364153)
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| Project Period (FY) |
2008 – 2010
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| Keywords | 癌性疼痛 / 神経因性疼痛 / グリア / 細胞再生 |
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| Research Abstract |
In this study, we elucidated effect of the spinal nerve-glia interaction on cancer pain and/or neuropathic pain of the rat regio infraorbitalis and studied it for the purpose of obtaining an underlying finding whether or not the treatment by the neurotrophy factor was effective. At first we made the inflammatory pain and cancer pain rat model that injected Freund's adjuvant or Walker 256 B into the rat regio infraorbitalis and gave antiphlogistic indomethacin to an inflammatory pain rat and a cancer pain rat to determine difference in both pain. Furthermore, we determined manifestation by the early period of onset of the c-fos gene in the merotomy of the neuropathic pain and the cancer pain rat. The pain behavior significantly inhibited it with each drug when COX-II inhibitor, p38MAPK inhibitor, microglial inactivator were given to the neuropathic pain and the cancer pain rat, respectively. In the neuropathic pain, activation of the spinal cord glutamate nervous system occurs early in
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the onset, and activation of p38-MAPK occurs successively, Synaptic transmission of the spinal nerre system was modified remarkably, and the microglia which was inflammation charge cells nearby activated it, and what it integrated it to be accompanied with COX-II, activation and BDNF (brain-derived neurotrophic factor) isolation of p38-MAPK, and developed in neuropathic pain became clear. We performed immunostaining of the trigeminal ganglion merotomy in GFAP, Iba1 to examine the microglia and astrocytic in neuropathic pain and the cancer pain rat contribution, respectively. Microglial activation was found early in the pain onset in both of the examination of the neuropathic pain and the cancer pain, and astrocytic activation was found late. Also, a significant decrease of cancer pain was found when subcutaneous injection of the microglial inactivator to a cancer pain rat was provided. By this result, It was found that spinal cord - microglial interaction was involved in both pain mechanisms of neuropathic pain and cancer pain. Less
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