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開催日 2014/9/11
時間 10:00 - 11:00
会場 Room J(313+314)
Chairperson(s) 中川 貴之 / Takayuki Nakagawa (京都大学医学部附属病院 薬剤部 / Department of Clinical Pharmacology and Therapeutics, Kyoto University Hospital, Japan)
鈴木 えみ子 / Emiko Suzuki (国立遺伝学研究所 構造遺伝学研究センター / Structural biology Center, National Institute of Genetics, Japan)

Intrathecal Administration of NMDA Activates Spinal Microglia and Production of Cytokines in Rats

  • O1-J-2-4
  • Li Li:1 Shan Ji:2 Yong Wang:2 Wenbin Li:2 
  • 1:Dept Sci & Tech, The Second Hospital of Hebei Medical University, Shijiazhuang, China 2:Hebei Medical University, China 

It has been shown that microglial cells in spinal cord dorsal horn can be activated by nociceptive stimuli and the activated microglial cells release various cytokines enhancing the nociceptive transmission. However, the mechanism underlying the activation of spinal microglia during nociceptive stimuli is not well defined. The present study was undertaken to investigate the role of NMDA receptor in the activation of spinal microglia. Spague-Dawley rats were intrathecally injected with NMDA, the selective NMDA receptor agonist. Mechanical withdrawal threshold, thermal withdrawal latency and tail flick latency to hot water immersion were observed to reflect pain behavior. The expression level of CD11b/c, a specific marker of microglia, in the dorsal horn of lumbar 4-5 spinal segments was examined to evaluate the activation of microglia by immunohistochemistry and western blot analysis. The generation of cytokines TNF-α and IL-1β was assessed by elisa. After treatment of NMDA, all rats produced a monophasic nociception characterized by decreased thermal withdrawal latency, mechanical withdrawal threshold and tail flick latency, indicating that pain and hyperalgesia were induced by NMDA. Immunohistochemistry displayed microglia with enlarged cell bodies, thickened and extended cellular processes. Western blot analysis showed that the expression level of CD11b/c was significantly up-regulated in time and dose-dependent manners. The up-regulation of CD11b/c expression was significantly inhibited by prior intrathecal injection of MK801, the selective antagonist of NMDA receptor. Elisa showed that TNF-α and IL-1β increased after the administration of NMDA, and the increase was inhibited by pretreatment of MK801. It can be concluded that intrathecal administration of NMDA activates spinal microglia and production of cytokines in rats, suggesting that NMDA receptor takes part in the mediation of spinal microglia activation pathological pain and hyperalgesia.

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