School of Biochemistry, Centre for Synaptic Plasticity, Biomedical Sciences Building, University of Bristol, University Walk, Bristol, BS8 1TD, UK; Centre for Neuroscience and Regenerative Medicine, Faculty of Science, University of Technology Sydney, Ultimo, NSW, Australia.
School of Biochemistry, Centre for Synaptic Plasticity, Biomedical Sciences Building, University of Bristol, University Walk, Bristol, BS8 1TD, UK.
Neuropharmacology. 2021 Sep 1;195:108569. doi: 10.1016/j.neuropharm.2021.108569. Epub 2021 Apr 26.
Epilepsy is caused when rhythmic neuronal network activity escapes normal control mechanisms, resulting in seizures. There is an extensive and growing body of evidence that the onset and maintenance of epilepsy involves alterations in the trafficking, synaptic surface expression and signalling of kainate and AMPA receptors (KARs and AMPARs). The KAR subunit GluK2 and AMPAR subunit GluA2 are key determinants of the properties of their respective assembled receptors. Both subunits are subject to extensive protein interactions, RNA editing and post-translational modifications. In this review we focus on the cell biology of GluK2-containing KARs and GluA2-containing AMPARs and outline how their regulation and dysregulation is implicated in, and affected by, seizure activity. Further, we discuss role of KARs in regulating AMPAR surface expression and plasticity, and the relevance of this to epilepsy. This article is part of the special issue on 'Glutamate Receptors - Kainate receptors'.
当节律性神经元网络活动逃脱正常的控制机制时，就会引起癫痫发作。有大量越来越多的证据表明，癫痫的发作和维持涉及到 kainate 和 AMPA 受体 (KAR 和 AMPAR) 的运输、突触表面表达和信号转导的改变。KAR 亚基 GluK2 和 AMPAR 亚基 GluA2 是其各自组装受体特性的关键决定因素。这两个亚基都受到广泛的蛋白质相互作用、RNA 编辑和翻译后修饰的影响。在这篇综述中，我们重点介绍了含有 GluK2 的 KAR 和含有 GluA2 的 AMPAR 的细胞生物学，并概述了它们的调节和失调如何与癫痫发作活动有关，并受其影响。此外，我们还讨论了 KAR 在调节 AMPAR 表面表达和可塑性中的作用，以及这与癫痫的相关性。本文是“谷氨酸受体- kainate 受体”特刊的一部分。
