首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Chemokine CCL7 regulates spinal phosphorylation of GluA1-containing AMPA receptor via interleukin-18 in remifentanil-induced hyperalgesia in rats
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Chemokine CCL7 regulates spinal phosphorylation of GluA1-containing AMPA receptor via interleukin-18 in remifentanil-induced hyperalgesia in rats

机译:趋化因子CCL7通过白细胞介素-18调节含有Glua1的AMPA受体的脊髓磷酸化,在大鼠中的verifentanil诱导的痛觉中

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Background: Remifentanil-induced hyperalgesia (RIH) may be a potential component for acute confusional state and chronic pain after surgery, but specific mechanism remains elusive. Chemokines and inflammatory mediators associated neuroinflammation is involved in central nociceptive sensitization. The contribution of AMPA receptor to excitatory synaptic transmission in pathologic pain has been indicated. This study investigated whether chemokine CCL7 modulated spinal phosphorylation of AMPA receptor via interleukin (IL)-18 in a rat model of RIH.
机译:背景:Remifentanil诱导的痛觉过敏症(RIH)可能是急性对抗状态和手术后慢性疼痛的潜在组成部分,但具体机制仍然难以捉摸。 趋化因子和炎症介质相关的神经引发剂涉及中央伤害性敏感性。 已经表明了AMPA受体在病理疼痛中兴奋性突触传递的贡献。 该研究研究了汝素蛋白(IL)-18在RIH的大鼠模型中的AMPA受体的趋化因子CCL7调节脊髓磷酸化。

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