小胶质细胞
周围神经损伤
痛觉过敏
医学
神经损伤
酵母多糖
伤害
外围设备
脊髓
麻醉
炎症
SNi公司
坐骨神经
中枢神经系统
神经科学
免疫学
内分泌学
内科学
化学
生物
受体
体外
精神科
水解
生物化学
酸水解
作者
Anna K. Clark,Clive Gentry,Elizabeth J. Bradbury,Stephen B. McMahon,Marzia Malcangio
标识
DOI:10.1016/j.ejpain.2006.02.003
摘要
Mounting evidence supports the hypothesis that spinal microglia modulate the development and maintenance of some chronic pain states. Here we examined the role of spinal microglia following both peripheral inflammatory insult and peripheral nerve injury. We observed significant ipsilateral dorsal horn microglia activation 2 weeks after injury and bilateral activation 50 days following nerve injury as well as 24 h following intraplantar zymosan but not intraplantar complete Freund's adjuvant (CFA). Ipsilateral but not contralateral microglia activation was associated with hind paw mechanical hyperalgesia. Spinal injection of the glial metabolic inactivator fluorocitrate attenuated ipsilateral hyperalgesia and bilateral spinal microglia activation after peripheral nerve injury. Intrathecal fluorocitrate reversed hyperalgesia after intraplantar zymosan and produced no reversal of CFA-induced hyperalgesia. These data suggest a role for spinal glia in the persistence of mechanical hyperalgesia following peripheral nerve injury. However, activation of spinal microglia contralaterally did not correlate to nociception. Furthermore, it would appear that the time course of microglia activation and their contribution to inflammatory pain is dependent on the inflammatory stimulus administered.
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