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在疼痛中,AMPA 型谷氨酸受体功能失调的新作用。

The emerging role of kainate receptor functional dysregulation in pain.

机构信息

Department of Anesthesiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.

Department of Neurobiology, Capital Medical University, Beijing, China.

出版信息

Mol Pain. 2021 Jan-Dec;17:1744806921990944. doi: 10.1177/1744806921990944.

DOI:10.1177/1744806921990944
PMID:33567997
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7883153/
Abstract

Pain is a serious clinical challenge, and is associated with a significant reduction in quality of life and high financial costs for affected patients. Research efforts have been made to explore the etiological basis of pain to guide the future treatment of patients suffering from pain conditions. Findings from studies using KA (kainate) receptor agonist, antagonists and receptor knockout mice suggested that KA receptor dysregulation and dysfunction may govern both peripheral and central sensitization in the context of pain. Additional evidence showed that KA receptor dysfunction may disrupt the finely-tuned process of glutamic acid transmission, thereby contributing to the onset of a range of pathological contexts. In the present review, we summarized major findings in recent studies which examined the roles of KA receptor dysregulation in nociceptive transmission and in pain. This timely overview of current knowledge will help to provide a framework for future developing novel therapeutic strategies to manage pain.

摘要

疼痛是一个严重的临床挑战,它会导致患者生活质量显著下降,并带来高昂的经济负担。研究人员一直在努力探索疼痛的病因基础,以指导未来对疼痛患者的治疗。使用红藻氨酸(KA)受体激动剂、拮抗剂和受体敲除小鼠进行的研究结果表明,KA 受体失调和功能障碍可能控制疼痛情况下的外周和中枢敏化。其他证据表明,KA 受体功能障碍可能破坏谷氨酸传递的精细调节过程,从而导致一系列病理情况的发生。在本综述中,我们总结了最近研究中关于 KA 受体失调在伤害性传递和疼痛中的作用的主要发现。这一及时的知识概述将有助于为未来开发新的治疗疼痛的策略提供框架。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e8e/7883153/191dc6c385ef/10.1177_1744806921990944-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e8e/7883153/8e3b6b302fc4/10.1177_1744806921990944-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e8e/7883153/4ec5a4cd4d60/10.1177_1744806921990944-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e8e/7883153/191dc6c385ef/10.1177_1744806921990944-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e8e/7883153/8e3b6b302fc4/10.1177_1744806921990944-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e8e/7883153/4ec5a4cd4d60/10.1177_1744806921990944-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e8e/7883153/191dc6c385ef/10.1177_1744806921990944-fig3.jpg

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本文引用的文献

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Front Synaptic Neurosci. 2020 Jul 10;12:26. doi: 10.3389/fnsyn.2020.00026. eCollection 2020.
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Seizure protein 6 controls glycosylation and trafficking of kainate receptor subunits GluK2 and GluK3.癫痫相关蛋白 6 控制了 kainate 受体亚基 GluK2 和 GluK3 的糖基化和转运。
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Kainate Receptor Activation Shapes Short-Term Synaptic Plasticity by Controlling Receptor Lateral Mobility at Glutamatergic Synapses.
病理性疼痛中环突触神经连接蛋白-神经黏连蛋白相互作用的调制。
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