神经病理性疼痛中交感神经与胶质细胞活化的相关性研究进展

Research Progress on the Correlation between Sympathetic Nerve Activation and Glial Cell Activation in Neuropathic Pain

摘要: 神经病理性疼痛，即由躯体感觉神经系统损伤或功能紊乱所继发的慢性疼痛综合征，流行病学数据显示其患病率已达7%~10%且呈持续攀升之势。值得注意的是，该病的病理机制迄今尚未被完全阐明，而传统干预手段的疗效亦存在明显局限。既往研究多将目光聚焦于神经元的核心地位，然近年来的证据表明，非神经元细胞(胶质细胞)和以及异常的交感神经活动，在NP的发生、演进乃至慢性化进程中均具有重要地位。本文旨在系统梳理交感神经与胶质细胞间的交互作用：一方面，交感神经可通过与外周神经异常耦合、调控中枢痛觉环路、以及在皮肤及脊髓内发生神经纤维靶向性发芽等途径，与感觉神经元建立功能联系，进而强化痛觉信号的传递；另一方面，脊髓胶质细胞在NP状态下可受炎症因子及伤害性信号分子激活，通过分泌多种生物活性物质、调控突触可塑性等方式参与痛觉敏化。尤为关键的是，二者借助神经免疫炎症反应及信号通路交叉对话，构建起双向调控网络，共同驱动疼痛的慢性化进程。通过对该领域研究进展的整合，本文为揭示NP发病新机制、推动特异性受体靶向或细胞表型调控类新型治疗策略的开发，提供必要的理论依据。

Abstract: Neuropathic Pain (NP) is a chronic pain syndrome caused by primary injury or dysfunction of the somatosensory nervous system, with a prevalence rate of 7% to 10% in the general healthy population and an increasing trend. Its complex pathological mechanisms have not been fully elucidated, and traditional therapeutic approaches have limited efficacy. Previous studies have mostly focused on the core role of neurons, while recent research has confirmed that non-neuronal cells (glial cells) and abnormal sympathetic nerve activity play crucial roles in the occurrence, development, and chronicization of NP. This article systematically reviews the interaction mechanisms between sympathetic nerves and glial cells (microglia, astrocytes) at the spinal cord level: Sympathetic nerves can form functional connections with sensory neurons through multiple pathways, including abnormal coupling in peripheral nerves, regulation of central pain circuits, and targeted sprouting of nerve fibers in the skin and spinal cord, thereby enhancing pain signal transmission. Spinal glial cells can be activated by inflammatory factors and nociceptive signaling molecules under NP conditions, and participate in pain sensitization by secreting bioactive substances and regulating synaptic plasticity. Through neuroimmune inflammatory responses and cross-talk of signaling pathways, the two form a bidirectional regulatory network that jointly drives the chronicization of pain. This article aims to integrate the research progress in this field, providing a theoretical basis for revealing new pathogenic mechanisms of NP and developing novel therapeutic strategies targeting specific receptors or cell phenotype regulation.