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

doi:10.1016/j.neuropharm.2021.108569

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^*

^*Corresponding author for this work

School of Biochemistry

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Abstract

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.

Original language	English
Article number	108569
Journal	Neuropharmacology
Volume	195
Early online date	26 Apr 2021
DOIs	https://doi.org/10.1016/j.neuropharm.2021.108569
Publication status	Published - 3 Jul 2021

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

abstract = "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.",

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T1 - Kainate and AMPA receptors in epilepsy

T2 - Cell biology, signalling pathways and possible crosstalk

AU - Henley, Jeremy M

AU - Nair, Jithin D

AU - Seager, Richard

AU - Yucel, Busra P

AU - Woodhall, Gavin

AU - Henley, Benjamin S

AU - Talandyte, Karolina

AU - Needs, Hope I

AU - Wilkinson, Kevin A

PY - 2021/7/3

Y1 - 2021/7/3

N2 - 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.

AB - 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.

U2 - 10.1016/j.neuropharm.2021.108569

DO - 10.1016/j.neuropharm.2021.108569

M3 - Article (Academic Journal)

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SN - 0028-3908

VL - 195

JO - Neuropharmacology

JF - Neuropharmacology

M1 - 108569

ER -

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

Abstract

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