突触发生
神经病理性疼痛
基因敲除
神经科学
神经传递
突触可塑性
兴奋性突触后电位
痛觉过敏
下调和上调
痛觉超敏
医学
化学
心理学
伤害
抑制性突触后电位
内科学
受体
基因
细胞凋亡
生物化学
作者
Yiling Wu,Qiaochu Fu,Xiaoxia Huang,Yifan Luo,Shengjun Wan,Minjing Peng,Shanchun Su,Xueqin Xu,Yang Li,Xiaohui Li,Dongsheng Sun,Changbin Ke
标识
DOI:10.1016/j.neuropharm.2021.108919
摘要
Neuropathic pain is the most common symptom for which patients seek medical attention. Existing treatments to control pain are largely ineffective because of poor understanding the underlying mechanisms. Synaptic plasticity is fundamental to the spinal sensitivity of neuropathic pain. In the present study, we showed that SNL induced significant allodynia and hyperalgesia as well as upregulation of Nwd1 and GluN2B, which were reversed by knockdown of NWD1. Electrophysiological experiments demonstrated that SNL enhanced synaptic transmission, which was prevented by knockdown of NWD1. In vitro experiments showed that knockdown of NWD1 inhibited dendritic growth and synaptogenesis. Taken together, our results suggest that NWD1 enhances synaptic transmission and contributes to the development of neuropathic pain by enhancing GluN2B synaptic expression and anchor and promoting excitatory synaptogenesis.
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