| Project/Area Number |
18390069
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Environmental physiology (including Physical medicine and Nutritional physiology)
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| Research Institution | Nagoya University |
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Principal Investigator |
MIZUMURA Kazue Nagoya University, Res. Inst. Environ. Med, Professor (00109349)
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| Co-Investigator(Kenkyū-buntansha) |
KOZAKI Yasuko Kinjo Galkuin Univ, Dept. Pharmacy, Associate Professor (20126882)
KATANOSAKA Kimiaki Nagoya University, Res. Inst Environ Med, Assistant Professor (50335006)
HONDA Takashi Fukushima Medical Univ, School of Nursing, Professor (20165608)
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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 |
¥15,000,000 (Direct Cost: ¥13,200,000、Indirect Cost: ¥1,800,000)
Fiscal Year 2007: ¥7,800,000 (Direct Cost: ¥6,000,000、Indirect Cost: ¥1,800,000)
Fiscal Year 2006: ¥7,200,000 (Direct Cost: ¥7,200,000)
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| Keywords | muscular mechanical hyperalgesia / bradykinin / COX2 / nerve growth factor (NGF) / delayed onset muscle soreness / ATP / lengthening contraction / muscle thin-fiber receptors / COX1 / 筋性疼痛 / 機械痛覚過敏 / プロスタグランジン |
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| Research Abstract |
To clarify the mechanism for the muscular mechanical hyperalgesia, following three points were examined using a rat model of delayed onset muscle soreness that was induced by loading lengthening contraction (LC). 1. Change of sensitizing substances in the muscle that is released by compression of the muscle or during contraction, and sensitization of muscle C-fiber receptors by these substances. 2. Change in ion channels and reception expressed in muscle C-fiber sensory receptor neurons. 3. Change in physical (mechanical) environment of muscle sensory receptors in edematous muscle after LC. We found: 1. ATP was released by compression of the muscle, but its amount was not different between the muscles before and 2 days after LC. ATP 0.1-100 μM rather suppressed the response of muscle C-fiber receptors to the mechanical stimulation. Administration of bradykinin receptor antagonists, Cox inhibitors and anti-NGF (nerve growth factor) antibody at different time points around LC revealed that bradykinin through B2 receptors and Cox-2 were involved in triggering the process to mechanical hyperalgesia, and that NGF was involved in maintenance of mechanical hyperalgesia. Corresponding to these observations expression of Cox-2 mRNA and protein increased during 0 12 hr after LC whereas NGF mRNA increased during 12 hr 2 days after LC. NGF facilitated the mechanical response of muscle thin-fiber receptors recorded in vitro, supporting the role of NGF in mechanical hyperalgesia after LC. 2. Suppression subtractive hybridization analysis of mRNA in DRGs after exercise revealed upregulation of RNAs of 65 substances. RTPCR of two of them, pain-related annexin A2 and calbindin 1, showed significant increase 2 days after LC. 3. The muscle 2 days after LC was by about 5% heavier, suggesting existence of edema after I.C. Immunohistochemistry of aquaporin 1 and 4 in muscle showed no consistent change after LC.
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