CONTINUOUS ADMINISTRATION OF NALOXONE INDUCED PROLIF-ERATION AND DIFFERENTIATION OF ENDOGENOUS OLIGODEN-DROCYTE PROGENITOR CELLS FOLLOWING SPINAL CORD INJURY

  • 伊藤 博隆
    Department of Neuro-physiology && Brain Science, Nagoya City University Graduate School of Medical Sciences
  • 飛田 秀樹
    Department of Neuro-physiology && Brain Science, Nagoya City University Graduate School of Medical Sciences
  • 増田 匡
    Department of Neuro-physiology && Brain Science, Nagoya City University Graduate School of Medical Sciences
  • 西野 仁雄
    Department of Neuro-physiology && Brain Science, Nagoya City University Graduate School of Medical Sciences

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説明

An opioid receptor antagonist naloxone has been considered pharmacologically benefical to endotoxin shock, experimental cerebral ischemia, and spinal cord injury. However, the mechanisms underlying these beneficial effects of naloxone are still not clear. In the present study, to investigate whether naloxone is effective in proliferation and differentiation of endogenous oligodendrocyte progenitor cells (OPCs) following spinal cord injury (SCI), a contusive SCI was first made in female Wistar rats with a weight (20 g, 2.5 mm diameter, 30 mm height) after laminectomy at Th 9/10 and then naloxone (dissolved in saline) was treated using osmotic pump (0. 1 mg/day, s.c.) for 7 days. Rats were sacrificed for immunohistochemical staining against oligodendorocyte progenitor markers (NG2, O4) and degraded myelin basic protein marker (MBP-D). The mean number of NG2-positive early immature OPCs in naloxone-treated sections was significantly increased compared with control at 3 and 9 days in the ventral white matter (VWM) after SCI. Although we can rarely detect 0 4-positive cells between 1 and 3 days after SCI, these cells significantly increased in the VWM between 9 and 14 days after SCI in naloxone-treated group compared with control. Additionally, in naloxone-treated group, the number of MBP-D-positive cells (at 1 day) was significantly decreased in the VWI. These data indicate that naloxone influences protective aspects of the secondary demyelinating response, a characteristic that is likely responsible for its ability to induce proliferation and differentiation of endogenous OPCs after SCI.

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