SAP102 通过锚定 NMDA 受体促进癌性骨痛大鼠模型中的痛觉过敏形成。
SAP102 contributes to hyperalgesia formation in the cancer induced bone pain rat model by anchoring NMDA receptors.
机构信息
Department of Anesthesiology, Bengbu Medical College, Bengbu, 233000, PR China; Department of Anesthesiology and Pain Medicine, The First Affiliated Hospital of Jiaxing University, Jiaxing, 314001, PR China.
Department of Anesthesiology, Chenzhou NO.1 People's Hospital, Chenzhou, 423000, PR China.
出版信息
Neurosci Lett. 2020 Jan 1;714:134595. doi: 10.1016/j.neulet.2019.134595. Epub 2019 Nov 1.
The pathogenesis of cancer induced bone pain (CIBP) is extremely complex, and glutamate receptor dysfunction plays an important role in the formation of CIBP. Synapse-associated protein 102 (SAP102) anchors glutamate receptors in the postsynaptic membrane. However, its effect on hyperalgesia formation in CIBP has not been clarified. This study investigated the role of SAP102 in the formation of hyperalgesia in rats with CIBP SAP102 is present in spinal dorsal horn neurons, but not in astrocytes or microglia. NMDAR-NR2B is localized with neurons. In addition, SAP102 and NMDAR-NR2B expression levels in spinal dorsal horn tissues were detected by Western blot and co-immunoprecipitation. Intrathecal injection of lentiviral vector of RNAi to knockdown SAP102 expression in the spinal dorsal horn significantly attenuated abnormal mechanic pain when compared to non-coding lentiviral vector. These findings indicate that SAP102 can anchor NMDA receptors to affect hyperalgesia formation in bone cancer pain.
癌症诱导性骨痛（CIBP）的发病机制极其复杂，谷氨酸受体功能障碍在 CIBP 的形成中起重要作用。突触相关蛋白 102（SAP102）将谷氨酸受体锚定在突触后膜上。然而，其在 CIBP 中痛觉过敏形成中的作用尚不清楚。本研究探讨了 SAP102 在 CIBP 大鼠痛觉过敏形成中的作用。SAP102 存在于脊髓背角神经元中，但不存在于星形胶质细胞或小胶质细胞中。NMDAR-NR2B 与神经元一起定位。此外，通过 Western blot 和共免疫沉淀检测脊髓背角组织中 SAP102 和 NMDAR-NR2B 的表达水平。鞘内注射 RNAi 慢病毒载体敲低脊髓背角中的 SAP102 表达，与非编码慢病毒载体相比，明显减轻异常机械性疼痛。这些发现表明，SAP102 可以锚定 NMDA 受体，从而影响骨癌痛中的痛觉过敏形成。
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