[1]张茹馨,高 强,郑祥德.NMDA受体NR2B亚基在疼痛形成中的作用机制[J].医学信息,2023,36(07):184-188.[doi:10.3969/j.issn.1006-1959.2023.07.038]
 ZHANG Ru-xin,GAO Qiang,ZHENG Xiang-de.The Mechanism of NMDA Receptor NR2B Subunit in Pain Formation[J].Journal of Medical Information,2023,36(07):184-188.[doi:10.3969/j.issn.1006-1959.2023.07.038]
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NMDA受体NR2B亚基在疼痛形成中的作用机制()
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医学信息[ISSN:1006-1959/CN:61-1278/R]

卷:
36卷
期数:
2023年07期
页码:
184-188
栏目:
综述
出版日期:
2023-04-01

文章信息/Info

Title:
The Mechanism of NMDA Receptor NR2B Subunit in Pain Formation
文章编号:
1006-1959(2023)07-0184-05
作者:
张茹馨高 强郑祥德
(1.川北医学院临床医学系,四川 南充 637000;2.达州市中心医院重症医学科,四川 达州 635000)
Author(s):
ZHANG Ru-xinGAO QiangZHENG Xiang-de
(1.Department of Clinical Medicine,North Sichuan Medical College,Nanchong 637000,Sichuan,China;2.Department of Intensive Care Medicine,Dazhou Central Hospital,Dazhou 635000,Sichuan,China)
关键词:
NR2B亚基NMDA受体疼痛
Keywords:
NR2B subunitNMDA receptorPain
分类号:
R441.1;R34
DOI:
10.3969/j.issn.1006-1959.2023.07.038
文献标志码:
A
摘要:
N-甲基-D-天冬氨酸(NMDA)受体是一种介导兴奋性神经递质传递的离子型谷氨酸受体。NMDA受体主要由7个亚基(NR1、NR2A、NR2B、NR2C、NR2D、NR3A、NR3B)组成。疼痛是一种由实际或潜在的组织损伤导致的不愉快的感觉和情绪体验。NMDA受体NR2B亚基参与大脑皮质区的疼痛信号传递和表达,在中枢敏化、痛觉过敏和突触的可塑性中有着重要的意义。NR2B亚基在中枢神经系统的过度表达与疼痛的形成密切相关,本文就NMDA受体NR2B亚基在疼痛形成中的作用机制作一综述,以期为疼痛的药物治疗带来新思路。
Abstract:
The N-methyl-D-aspartate (NMDA) receptor is an ionotropic glutamate receptor that mediates excitatory neurotransmitter transmission. The NMDA receptor is composed of seven main subunits (NR1, NR2A, NR2B, NR2C, NR2D, NR3A, NR3B). Pain is an unpleasant sensory and emotional experience caused by actual or potential tissue damage.T he NMDA receptor NR2B subunit is involved in pain signaling and expression in the cerebral cortex area, which has important significance in central sensitization, hyperalgesia and synaptic plasticity. The overexpression of NR2B subunits in the central nervous system is closely related to the formation of pain, and this article reviews the mechanism of NMDA receptor NR2B subunits in pain formation, in order to bring new ideas for the drug treatment of pain.

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更新日期/Last Update: 1900-01-01