| Project/Area Number |
18613020
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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 |
Pain science
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| Research Institution | Aichi Medical University |
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Principal Investigator |
KUMAZAWA Takao Aichi Medical University, School of Medicine, Department of Algesiology, Professor (20022775)
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| Co-Investigator(Kenkyū-buntansha) |
HONDA Takashi Fukushima Medical University, School of Nursing, Professor (20165608)
OHISHI Hitoshi Aichi Medical University, School of Medicine, Department of Anatomy, Associate Professor (00252461)
橋本 辰幸 愛知医科大学, 医学部, 助手 (80367763)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥4,060,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥360,000)
Fiscal Year 2007: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2006: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | chronic pain / animal model / muscle damage / immunohistochemistry / molecular biology / autonomic nervous system / spinal cord / glia / 筋障害 / 痛み |
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| Research Abstract |
In this study, two types of chronic pain animal models (myo-nociceptive model, cast-immobilization model) we had developed were used. The characteristics of these models are: 1) direct nerve injuries are not given; 2) bilateral wide-spread long-lasting pain behaviors are developed. The purpose of this study is to clarify the chronic pain mechanisms of these models.
1. In the chronic pain phase of these models, the contralateral hyperalgesia in the hind-paw was not affected by the ipsilateral sciatic nerve block. This result suggests the implication of central plasticity.
2. In the L4 dorsal horn of the cast-immobilization model, the microglias at the early phase after cast-removal and the astrocytes at the chronic pain phase had activated. When the paw hyperalgesia tend to attenuate, the activation of both types of spinal glial cells reduced. In the coccygeal cord, the microglial activation appeared in retard of that in the L4. The implication of spinal glial cells is suggested in this model. As the preliminary examination, IL-6 and BDNF mRNA expressions in spinal cord and muscles were determined by PCR.
3. In the cast-immobilization model, the autonomic parameters (blood pressure, heart rate) were telemetrically recorded, The sympathetic activity was augmented during cast-immobilization period and then decreased below the normal level while persisting pain behavior continued. In the chronic pain condition, the autonomic reactivities to cold-exposure were higher than in normal. Autonomic dysfunction in the chronic pain patients (e.g. CRPS type-I) is reported, so this model may be a partial explanation for those pathogenic conditions.
4. In the myo-nociceptive model, the treatment to young-age was not produced chronic pain behaviors. It is suggested any factors as a trigger to chronic pain may be immature.
5. Both of the minocycline injection and the treadmill exercise tended to decrease pain behaviors, though reexamination should be required.
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