Kainate receptors in the hippocampus

• Published in: The European journal of neuroscience Vol. 39; no. 11; pp. 1835 - 1844
• Main Authors: Carta, Mario, Fièvre, Sabine, Gorlewicz, Adam, Mulle, Christophe
• Format: Journal Article
• Language: English
• Published: France Blackwell Publishing Ltd 01.06.2014; Wiley
• Subjects: Animals; development; epilepsy; glutamate receptors; Hippocampus - growth & development; Hippocampus - metabolism; Hippocampus - physiology; Humans; Life Sciences; Neuronal Plasticity; Receptors, Kainic Acid - genetics; Receptors, Kainic Acid - metabolism; synapse; Synapses - metabolism; Synapses - physiology; synaptic plasticity; epilepsy; development; synapse; synaptic plasticity; glutamate receptors
• ISSN: 0953-816X; 1460-9568
• DOI: 10.1111/ejn.12590

Kainate receptors (KARs) consist of a family of ionotropic glutamate receptors composed of the combinations of five subunits, GluK1–GluK5. Although KARs display close structural homology with AMPA receptors, they serve quite distinct functions. A great deal of our knowledge of the molecular and functional properties of KARs comes from their study in the hippocampus. This review aims at summarising the functions of KARs in the regulation of the activity of hippocampal synaptic circuits at the adult stage and throughout development. We focus on the variety of roles played by KARs in physiological conditions of activation, at pre‐ and postsynaptic sites, in different cell types and through either metabotropic or ionotropic actions. Finally, we present some of the few attempts to link the role of KARs in the regulation of local hippocampal circuits to the behavioural functions of the hippocampus in health and diseases. This review summarises the functions of ionotropic glutamate receptors of the kainate type (KARs) in the hippocampus in health and diseases. KARs regulate the activity of hippocampal synaptic circuits at the adult stage and throughout development. We focus on the variety of roles played by KARs in physiological conditions of activation by endogenously‐released glutamate acting at either pre‐ or postsynaptic sites, through either metabotropic or ionotropic actions.