| Project/Area Number |
12671501
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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 | Dokkyo University School of Medicine |
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Principal Investigator |
TAKANO Yoshito Dokkyo University School of Medicine, Professor, 医学部, 教授 (10134701)
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| Co-Investigator(Kenkyū-buntansha) |
ARAI Takero Dokkyo University School of Medicine, Assistant Professor, 医学部, 助手 (00276148)
KUNO Yuichiro Dokkyo University School of Medicine, Assistant Professor, 医学部, 助手 (20275738)
TAKANO Manami Dokkyo University School of Medicine, Associate Professor, 医学部, 講師 (70204352)
SATO Eiru Dokkyo University School of Medicine, Assistant Professor, 医学部, 助手 (60301462)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2002: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2001: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2000: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | neuropathic pain / dorsal horn neuaron / hyperalgesia / allodynia / apoptosis / 免疫抑制薬 / 脊髄ニューロン |
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| Research Abstract |
Hyperalgesia or allodynia after nerve injury is often refractory to conventional therapies. Neuronal death after nerve injury has been suggested. We examined the spinal cord sliced stained by anti-ssDNA (single stranded DNA) staining which exhibits early stage of apoptosis in rats with nerve injury. After admitted by Institutional Ethical Committee of Animal Experiments, left L5 spinal nerve of male Sprague-Dawley rat (200-250g) was tightly ligated according to the method described by Kim and Chung (1992). Sham operated rats were assigned to the control group. Thermal nociceptive thresholds were measured by paw withdrawal latency using a radiant heat source applied to dorsal surface of the paw. Tactile allodynia was measured by von Frey filament test. Paraformaldehyde-fixed spinal cord was extirpated 3 weeks after the injury. Cervical and lumbar spinal cord was sliced for microscopic examination. SsDNA positive cells in the area of 0.2mm X 0.14mm were counted in bilateral superficial d
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orsal horn and middle of ventral horn from each side. After nerve injury, mild, but significant thermal hyperalgesia and allodynia have developed on the paw of nerve-ligated side. Average baseline count of ssDNA positive cells in the cervical dorsal horn was 5.4 (left: sham operated side) and 5.6 (right). Mean count in lumbar cord was 5.6 (left) and 5.3 (right). Three weeks after the nerve injury, positive cell counts in cervical cord was 21.3 (left: injured side) and 13.8 (right). Positive cell in lumbar cord was 20.8 (left) and 13.9 (right). The increases in the cell count in both cervical and lumbar dorsal horn were statistically significant and cell counts in the injured side was significantly larger than non-injured side in both cervical and lumbar dorsal horn. In the ventral horn, positive cell increased by about 30% in both sides. After nerve injury, considerable number of cells in the spinal medulla dies by a mechanism of apoptosis. This irreversible change may underlie the plastic change in spinal nociceptive transmission and long lasting symptoms of neuropathic pain. Less
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