Neuroscience and Mental Health Institute and Department of Pharmacology, University of Alberta, Edmonton, Alberta T6G 2H7, Canada.
Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta T6G 2H7, Canada.
J Neuroimmunol. 2021 May 15;354:577529. doi: 10.1016/j.jneuroim.2021.577529. Epub 2021 Feb 25.
Peripheral nerve injury frequently evokes chronic neuropathic pain. This is initiated by a transient inflammatory response that leads to persistent excitation of dorsal root ganglion (DRG) neurons by inflammatory cytokines such as interleukin 1β(IL-1β). In non-neuronal cells such as lymphocytes, interleukin 1 exerts actions at attomolar (aM; 10 M) concentrations. We now report that DRG neurons in defined-medium, neuron-enriched culture display increased excitability following 5-6 d exposure of 1aM IL-1β. This response is mediated in part by type 1 interleukin receptors and involves decreased function of putative K1.1 channels. This finding provides new insights into the neuroimmune interactions responsible for neuropathic pain.
外周神经损伤常引起慢性神经性疼痛。这种疼痛是由短暂的炎症反应引起的，炎症反应导致白细胞介素 1β（IL-1β）等炎症细胞因子持续兴奋背根神经节（DRG）神经元。在淋巴细胞等非神经元细胞中，白细胞介素 1 在飞摩尔（aM；10 M）浓度下发挥作用。我们现在报告说，在含有特定培养基的神经元丰富培养物中，DRG 神经元在 1aM IL-1β暴露 5-6 天后显示兴奋性增加。这种反应部分是由 1 型白细胞介素受体介导的，涉及假定的 K1.1 通道功能降低。这一发现为导致神经性疼痛的神经免疫相互作用提供了新的见解。
