2004 Fiscal Year Final Research Report Summary
Mechanisms of Pain Transmission in the Painful States of Spinal Cord Injury and Peripheral Nerve Damage
| Project/Area Number |
14571455
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
OMOTE Keiichi Sapporo Medical University, School of Medicine Department of Anesthesiology, Associate Professor, 医学部, 助教授 (60185676)
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| Co-Investigator(Kenkyū-buntansha) |
KAWAMATA Tomoyuki Sapporo Medical University, School of Medicine Department of Anesthesiology, Instructor, 医学部, 助手 (80336388)
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| Project Period (FY) |
2002 – 2004
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| Keywords | Spinal Gord Iniuxy / COX-1 / COX-2 / Peripheral Nerve Iniury / Hyperalgesia / Prostaglandine / プロスタグランジン / 一酸化窒素 |
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| Research Abstract |
The models of spinal cord injury and peripheral axotomy were used Painfull behavioral assessments including flinching, hyperalgesia to thermal and mechanical stimuli, touch-evoked allodynia were performed. Following these behavioral assessments, expressions of cydooxygenase (COX)-1 and -2 proteins were measured in the lumbar dorsal root ganglions and lumbar spinal cord, using western blotting assay In addition, concentrations of prostaglandin (PG) E2 and 12 were measured using enzyme immunoassays, and concentration of nitric oxide (NO) was measured using high performance liquid chromatography (HPLC). NO synthase (NOS) inhibitor, L-NMMA was perfused in order to examine the effects of NO On PG. production in the painful states of spinal cord injury and peripheral nerve injury.
Behavioral Assessments: Prominent hyperalgesia (lowering escape thresholds) were observed 5 days after spinal cord injury and 4 days after peripheral nerve injury. Hyperalgesia continued for about 1 month.
Expression
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of COX: The proteins of COX-1 and COX-2 were limited in dorsal root ganglia and spinal cord in the normal rats. Following spinal cord injury, COX expressions were observed 3 days after the injury, and significant increase in COX proteins were observed 5 days after the injury. At the above site of the injury, COX-2 protein remarkably increased, compared with COX-1 protein. In peripheral nerve injury model, both OOX-1 and -2 proteins increased in the ipsilateral side of dorsal root ganglia and spinal cord.
Production of PGs and Nitric oxide: In peripheral nerve injury model, concentrations of PGE2 and PGI2 increased 4 days after the injury, and NO concentration was also increased 3 days after the injury. L-NMMA perfusion suppressed the production of NO production and also suppressed the expression of COX-2 protein, resulting in inhibiting PGs production.
These data suggest that in spinal cord injury, COX expression increases at the level of the injured spinal cord which contributes to production of PGs, resulting in establishment of painful states. In peripheral nerve injury, NO enhances to express the COX-2 protein which contributes to production of PGs, resulting in potentiation of painful states. Less
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