Department of Physiology, College of Korean Medicine, Daegu Haany University, Daegu, Republic of Korea.
Department of Neurobiology and Anatomy, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Neural Plast. 2017;2017:2480689. doi: 10.1155/2017/2480689. Epub 2017 Aug 29.
The hyperactive state of sensory neurons in the spinal cord enhances pain transmission. Spinal glial cells have also been implicated in enhanced excitability of spinal dorsal horn neurons, resulting in pain amplification and distortions. Traumatic injuries of the neural system such as spinal cord injury (SCI) induce neuronal hyperactivity and glial activation, causing maladaptive synaptic plasticity in the spinal cord. Recent studies demonstrate that SCI causes persistent glial activation with concomitant neuronal hyperactivity, thus providing the substrate for central neuropathic pain. Hyperactive sensory neurons and activated glial cells increase intracellular and extracellular glutamate, neuropeptides, adenosine triphosphates, proinflammatory cytokines, and reactive oxygen species concentrations, all of which enhance pain transmission. In addition, hyperactive sensory neurons and glial cells overexpress receptors and ion channels that maintain this enhanced pain transmission. Therefore, post-SCI neuronal-glial interactions create maladaptive synaptic circuits and activate intracellular signaling events that permanently contribute to enhanced neuropathic pain. In this review, we describe how hyperactivity of sensory neurons contributes to the maintenance of chronic neuropathic pain via neuronal-glial interactions following SCI.
脊髓感觉神经元的过度活跃状态增强了疼痛的传递。脊髓神经胶质细胞也被认为与脊髓背角神经元的兴奋性增强有关，导致疼痛放大和扭曲。神经系统的创伤性损伤，如脊髓损伤（SCI），会引起神经元过度活跃和神经胶质激活，导致脊髓中的适应性突触可塑性改变。最近的研究表明，SCI 会导致持续的神经胶质激活和伴随的神经元过度活跃，从而为中枢神经性疼痛提供了基础。过度活跃的感觉神经元和激活的神经胶质细胞会增加细胞内和细胞外谷氨酸、神经肽、三磷酸腺苷、促炎细胞因子和活性氧物质的浓度，所有这些都会增强疼痛的传递。此外，过度活跃的感觉神经元和神经胶质细胞过度表达受体和离子通道，维持这种增强的疼痛传递。因此，SCI 后神经元-神经胶质相互作用会产生适应性突触回路，并激活细胞内信号事件，这些事件会永久促进神经病理性疼痛的增强。在这篇综述中，我们描述了感觉神经元的过度活跃如何通过 SCI 后的神经元-神经胶质相互作用，对慢性神经病理性疼痛的维持产生影响。
