神经病理性疼痛
小胶质细胞
神经科学
伤害
调解人
趋化因子
医学
免疫系统
炎症
心理学
免疫学
受体
内科学
作者
Michael Thacker,Anna K. Clark,Thomas Bishop,John Grist,Ping K. Yip,Lawrence Moon,Steve Thompson,Fabien Marchand,Stephen B. McMahon
标识
DOI:10.1016/j.ejpain.2008.04.017
摘要
While neuroimmune interactions are increasingly recognized as important in nociceptive processing, the nature and functional significance of these interactions is not well defined. There are multiple reports that the activation of spinal microglia is a critical event in the generation of neuropathic pain behaviors but the mediators of this activation remain disputed. Here we show that the chemokine CCL2, produced by both damaged and undamaged primary sensory neurons in neuropathic pain states in rats, is released in an activity dependent manner from the central terminals of these fibres. We also demonstrate that intraspinal CCL2 in naïve rats leads to activation of spinal microglia and neuropathic pain-like behavior. An essential role for spinal CCL2 is demonstrated by the inhibition of neuropathic pain behavior and microglial activation by a specific neutralising antibody to CCL2 administered intrathecally. Thus, the neuronal expression of CCL2 provides a mechanism for immune activation, which in turn regulates the sensitivity of pain signaling systems in neuropathic pain states.
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