背景:中枢神经突触膜相关鸟苷酸激酶 (membrane-associated guanylate kinase, MAGUK)蛋白家族包含4种突触相关蛋白:PSD-93、PSD-95、SAP-102、SAP-97,它们参与调节谷氨酸突触信号传递,与学习记忆和疼痛等有关。目的:综述神经突触MAGUK锚定蛋白与疼痛相关受体和分子的相互作用及其在疼痛信号调节及传递中的作用。内容:神经突触M AGUK锚定蛋白可通过与N-甲基-D-天冬氨酸(N-methyl-D-aspartate, NMDA) 受体、神经元型一氧化氮合酶(neuronal nitric oxide synthase, nNOS)、使君子酸 (α-amino-3-hydroxy-5-methy-4-isoxazole propionate, AMPA)受体以及突触细胞粘附分子(Synaptic cell-adhesion molecules, SynCAM)等相互作用参与调节疼痛信号在突触的传递,影响突触传递强度。趋向:干扰神经突触MAGUK锚定蛋白与疼痛相关受体和重要分子间的相互作用可影响疼痛信号在突触的传递,是疼痛治疗的新靶点。
Background: A family of membrane-associated guanylate kinases (MAGUKs) in central nerve system contains 4 kinds of synapses-associated proteins: PSD-93、PSD-95、SAP-102、SAP-97. They are involved in modulating synaptic trafficking of glutamate receptors and have a tight relationship with pain, learning and memory. Objective: Reviewing the interactions between the synaptic MAGUK scaffolding proteins and the receptors、molecules involved in pain and the roles of which in pain signal modulation and transmission. Content: Synaptic MAGUK scaffolding proteins are involved in modulating pain signal transduction in synapses by interacting with NMDAR, nNOS, AMPAR, SynCAM and other molecules. Trend: Disruption of the interactions between the synaptic MAGUK scaffolding proteins and the receptors or molecules involved in pain can influence pain signal transduction in synapses, suggesting a new target for the treatment of pain.
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