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首页> 外文期刊>The European Journal of Neuroscience >Evidence that exogenous and endogenous fractalkine can induce spinal nociceptive facilitation in rats.
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Evidence that exogenous and endogenous fractalkine can induce spinal nociceptive facilitation in rats.

机译：外源性和内源性fractalkine可以诱导大鼠脊髓伤害感受性促进的证据。

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Recent evidence suggests that spinal cord glia can contribute to enhanced nociceptive responses. However, the signals that cause glial activation are unknown. Fractalkine (CX3C ligand-1; CX3CL1) is a unique chemokine expressed on the extracellular surface of spinal neurons and spinal sensory afferents. In the dorsal spinal cord, fractalkine receptors are primarily expressed by microglia. As fractalkine can be released from neurons upon strong activation, it has previously been suggested to be a neuron-to-glial signal that induces glial activation. The present series of experiments provide an initial investigation of the spinal pain modulatory effects of fractalkine. Intrathecal fractalkine produced dose-dependent mechanical allodynia and thermal hyperalgesia. In addition, a single injection of fractalkine receptor antagonist (neutralizing antibody against rat CX3C receptor-1; CX3CR1) delayed the development of mechanical allodynia and/or thermal hyperalgesia in two neuropathic pain models: chronic constriction injury (CCI) and sciatic inflammatory neuropathy. Intriguingly, anti-CX3CR1 reduced nociceptive responses when administered 5-7 days after CCI, suggesting that prolonged release of fractalkine may contribute to the maintenance of neuropathic pain. Taken together, these initial investigations of spinal fractalkine effects suggest that exogenous and endogenous fractalkine are involved in spinal sensitization, including that induced by peripheral neuropathy.
机译：最近的证据表明，脊髓神经胶质细胞可以促进伤害性反应。但是，导致胶质细胞激活的信号是未知的。 Fractalkine（CX3C配体-1; CX3CL1）是一种独特的趋化因子，表达于脊髓神经元和脊髓感觉传入细胞的细胞外表面。在背脊髓中，fractalkine受体主要由小胶质细胞表达。由于fractalkine可以在强烈激活后从神经元中释放出来，因此以前已经提出它是诱导神经胶质激活的神经元到神经胶质信号。本系列实验提供了对fractalkine的脊髓痛调节作用的初步研究。鞘内fractalkine产生剂量依赖性机械异常性疼痛和热痛觉过敏。此外，在两种神经性疼痛模型中，单次注射fractalkine受体拮抗剂（针对大鼠CX3C受体1的中和抗体; CX3CR1）延迟了机械性异常性疼痛和/或热痛觉过敏的发展：慢性收缩性损伤（CCI）和坐骨神经炎性神经病。有趣的是，抗CX3CR1在CCI后5-7天给药时可降低伤害性反应，表明fractalkine的延长释放可能有助于维持神经性疼痛。综上所述，这些对脊柱fractalkine影响的初步研究表明，外源性和内源性fractalkine参与了脊柱敏化，包括周围神经病引起的敏化。

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