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中文摘要：
骨肿瘤患者疼痛剧烈，临床上还缺乏疗效显著且副作用较小的治疗方法。N-甲基-D-天冬氨酸（NMDA）受体介导的脊髓水平中枢敏化是骨癌痛发生的重要机制之-。NR2B亚基C末端的氨基酸残基可特异性地与突触后致密蛋白95（PSD-95）的PDZ2结构域结合，有利于NMDA受体聚集于突触后致密区，并抑制NMDA受体内化，使含有NR2B哑基的NMDA受体在突触后致密区表达增多，介导了中枢敏化的发生。
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