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Role of spinal microglia in rat models of peripheral nerve injury and inflammation.

机译:脊髓小胶质细胞在大鼠周围神经损伤和炎症模型中的作用。

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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.
机译:越来越多的证据支持了脊髓小胶质细胞调节某些慢性疼痛状态的发展和维持的假说。在这里,我们研究了周围小炎症和周围神经损伤后脊髓小胶质细胞的作用。我们观察到损伤后2周有明显的同侧背角小胶质细胞活化,神经损伤后50天以及足底内酵母聚糖24小时后双侧活化,但足底内完全弗氏佐剂(CFA)未见。同侧而非对侧小胶质细胞活化与后爪机械性痛觉过敏相关。脊髓神经胶质代谢灭活剂氟柠檬酸盐的注射减轻了周围神经损伤后同侧痛觉过敏和双侧脊髓小胶质细胞的活化。鞘内注射zymosan后鞘内注射氟柠檬酸可逆转痛觉过敏,并且不会逆转CFA诱导的痛觉过敏。这些数据表明脊髓胶质细胞在周围神经损伤后持续的机械性痛觉过敏中起作用。但是,对侧脊髓小胶质细胞的激活与伤害感受无关。此外,似乎小胶质细胞活化的时间过程及其对炎性疼痛的贡献取决于所给予的炎性刺激。

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