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

Jeremy M Henley, Jithin D Nair, Richard Seager, Busra P Yucel, Gavin Woodhall, Benjamin S Henley, Karolina Talandyte, Hope I Needs, Kevin A Wilkinson

Research output: Contribution to journalReview articlepeer-review


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'.

Original languageEnglish
Article number108569
Early online date26 Apr 2021
Publication statusPublished - 1 Sept 2021

Bibliographical note

© 2021, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/

Funding: We are grateful to the BBSRC (BB/R00787X/1), Wellcome Trust (220799/Z/20/Z) and Leverhulme Trust (RPG-2019-191) for financial support.


  • AMPA receptor
  • Synaptic Plasticity
  • epilepsy
  • glutamate receptors
  • kainate receptor
  • receptor trafficking
  • Glutamate receptors
  • Epilepsy
  • Synaptic plasticity
  • Receptor trafficking
  • Kainate receptor


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