摘要
背景中枢神经突触膜相关鸟苷酸激酶(membrane-associatedguanylatekinase,MAGUK)蛋白家族包含4种突触相关蛋白:PED-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之间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MAGUK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(neuronalnitricoxidesynthase,nNOS)、使君子酸(a-amino-3-hydroxy-5.nlethy4_isoxazolepropionate,AMPA)受体以及突触细胞黏附分子(synaptiecell-adhesionmolecules,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 nervous 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 associate with pain, learning and memory. Objective To review the interactions between the synaptic MAGUK scaffolding proteins and the receptors.molecules involved in pain and the roles of synaptic MAGUK scaffolding proteins 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.
出处
《国际麻醉学与复苏杂志》
CAS
2013年第3期273-276,280,共5页
International Journal of Anesthesiology and Resuscitation
基金
国家自然科学基金(81171055)
北京市自然科学基金(7112054)
教育部新世纪优秀人才支持计划(NCET-10-0014)