从“神经胶质细胞-神经元”互动角度探讨慢性疼痛的发生与维持机制

Mechanism of chronic pain development and maintenance from the perspective of"glia-neuron"interaction

神经元的可塑性变化是介导痛觉敏化的主要机制之一,痛觉敏化导致的慢性疼痛持续状态严重影响病人的生活质量。大量研究揭示了神经胶质细胞与神经元之间的密切联系、相互作用、共同参与慢性疼痛的调节。既往的研究多集中于激活的神经元或神经胶质细胞对慢性疼痛的调控作用,而两种细胞之间的信息传递在之后逐渐受到关注。近年来研究提示,神经胶质细胞与神经元通过多种神经递质、趋化因子、促炎症细胞因子作用于相应受体参与慢性疼痛的发生与维持。本文以细胞因子为切入点,对神经胶质细胞-神经元交互参与慢性疼痛的发生与维持机制进行综述,期望为神经炎症介导慢性疼痛的细胞分子治疗策略提供多角度、全方位理论参考。

Plasticity changes in neurons are one of the main mechanisms mediating nociceptive sensitization,and the persistence of chronic pain due to nociceptive sensitization seriously affects patients'quality of life.A large number of studies have revealed the close connection and interaction between glial cells and neurons,which are jointly involved in the regulation of chronic pain.Previous studies have mostly focused on the role of activated neurons or glial cells in the regulation of chronic pain,while the information transfer between the two cells has gradually received attention afterwards.Recent studies suggest that glial cells and neurons are involved in the development and maintenance of chronic pain through the action of various neurotransmitters,chemokines,and pro-inflammatory cytokines on the corresponding receptors.In this paper,we take cytokines as an entry point to review the mechanism of glia-neuron interaction in the development and maintenance of chronic pain,hoping to provide a multi-faceted and all-encompassing theoretical reference for cellular and molecular therapeutic strategies for neuroinflammation-mediated chronic pain.