背景 Neuroligin1是突触细胞黏附分子（synaptic cell adhesion molecules, SynCAM）的一种，与Neurexin1β及突触后膜致密蛋白95（postsynaptic density protein 95, PSD-95）相结合形成跨突触复合物，这一跨突触信号可以中介使君子酸（a-amino-3-hydroxy-5-methyl-4-isoxazole-propionate, AMPA）受体亚基突触靶向和突触前囊泡释放，在学习、记忆和疼痛中均具有重要作用。 目的 对Neuroligin1与突触活动的相互作用进行回顾与总结。 内容 Neuroligin1可通过调节AMPA受体、N?蛳甲基-D-天冬氨酸（N-methyl-D-aspartic acid, NMDA）受体的突触靶向来参与到突触活动中；相应的，突触活动也能诱导Neuroligin1的裂解和磷酸化，使突触活动趋于平衡。 趋向 通过下调Neuroligin1的表达或干扰其与PSD-95蛋白或Neurexin1β的相互作用，可间接抑制AMPA受体的功能，是未来疼痛治疗的研究方向。
Background Neuroligin1 is one of the synaptic cell adhesion molecule(SynCAM), which can combine with Neurexin1β and postsynaptic density protein 95(PSD-95) to form trans-synaptic complex. This trans-synaptic complex serves as a critical component involved in the synaptic targeting of a-amino-3-hydroxy-5-methyl-4-isoxazole-propionate(AMPA) receptors and releasing of the synaptic vesicles, therefore, plays an important role in learning, memory, and pain. Objective In this review, we will bring together the evidence showing the interaction between Neuroligin1 and synaptic activity. Content By facilitating synaptic targeting of AMPA receptors and N-methyl-D-aspartic acid(NMDA) receptors and neurotransmitter release, Neuroligin1 enhances synaptic transmission and plasticity. Conversely, altered synaptic activity triggers the cleavage and phosphorylation of Neuroligin1. Through the reciprocal interactions Neuroligin1 balances the function of excitatory synapses. Trend Down-regulation of Neuroligin1 expression or interfering the interaction between Neuroligin1 and PSD-95 or Neurexin1β may be a new approach for pain management.
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