Kainate and AMPA receptors in epilepsy: Cell biology, signalling pathways and possible crosstalk

NEUROPHARMACOLOGY

卷:195

Review

Henley, Jeremy M.^1,2  Nair, Jithin D.¹  Seager, Richard¹  Yucel, Busra P.¹  Woodhall, Gavin³  Henley, Benjamin S.⁴  Talandyte, Karolina¹  Needs, Hope I.¹  Wilkinson, Kevin A.¹ 

[1] Univ Bristol, Ctr Synapt Plast, Sch Biochem, Biomed Sci Bldg, Bristol BS8 1TD, Avon, England

[2] Univ Technol Sydney, Fac Sci, Ctr Neurosci & Regenerat Med, Ultimo, NSW, Australia

[3] Aston Univ, Sch Life & Hlth Sci, Birmingham B4 7ET, W Midlands, England

[4] Newcastle Univ, Med Sch, Fac Med Sci, Framlington Pl, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England

关键词: AMPA receptor;    Kainate receptor;    Epilepsy;    Receptor trafficking;    Synaptic plasticity;    Glutamate receptors;   

DOI  :  10.1016/j.neuropharm.2021.108569

来源: Elsevier

【 摘 要 】

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 posttranslational modifications. In this review we focus on the cell biology of GluK2-containing KARs and GluA2containing 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'.

【 授权许可】

Free