背根神经节表达的N-甲基-D-天冬氨酸受体在神经病理性疼痛中的作用

Research Progress of Dorsal Root Ganglion N-Methyl-D-Aspartic Acid Receptor in Neuropathic Pain

神经病理性疼痛(Neuropathic Pain,NP)是由躯体感觉神经系统的损伤或疾病直接造成的疼痛,如多发性神经病、带状疱疹后神经痛、三叉神经痛和卒中后疼痛.目前,NP的发病机制尚不明确,越来越多的学者认为中枢敏感化是慢性疼痛发生和维持所必需的.而背根神经节(Dorsal Root Ganglion,DRG)和脊髓背角突触的兴奋性及可塑性改变是中枢敏感化的关键.研究表明,中枢神经系统(Central Nervous System,CNS)中N-甲基-D-天冬氨酸受体(N-methyl-D-aspartic Acid Receptor,NMDAR)激活是中枢敏化所必需的,这一现象包括动物模型中NP样体征的各种病理生理机制.脊髓中的NMDAR被谷氨酸或N-甲基-D-天冬氨酸(N-Methyl-D-aspartic Acid,NMDA)激活产生伤害感受或行为痛觉过敏,而其作用可被NMDAR拮抗剂阻断.本文将综述DRG中的NMDAR在NP中的研究进展,供从事相关领域研究的学者参考.

Neuropathic pain(NP)is caused directly by injury or disease of the somatosensory nervous system,such as polyneuropathy,postherpetic neuralgia,trigeminal neuralgia and post-stroke pain.At present,the pathogenesis of NP is still unclear,and continuously increasing scholars believe that central sensitization is necessary for the occurrence and maintenance of chronic pain.The neuroexcitability of the dorsal root ganglion(DRG)and the plasticity of synapses in the dorsal horn of the spinal cord are key to central sensitization.Previous studies have shown that activation of NMDA receptor(N-methyl-D-aspartic Acid Receptor,NMDAR)in the central nervous system(CNS)is required for central sensitization,a phenomenon that includes various pathophysiological mechanisms for NP-like signs in animal models.NMDAR in the spinal cord is activated by glutamate or NMDA to produce nociceptive or behavioral hyperalgesia,whose effects are blocked by NMDAR antagonists.This article will review the research progress of NMDAR in DRG in neuropathic pain.