Abstract
N-Methyl-d-Aspartate Receptors (NMDARs) are ionotropic glutamate-gated receptors. NMDARs are tetramers composed by several homologous subunits of GluN1-, GluN2-, or GluN3-type, leading to the existence in the central nervous system of a high variety of receptor subtypes with different pharmacological and signaling properties. NMDAR subunit composition is strictly regulated during development and by activity-dependent synaptic plasticity. Given the differences between GluN2 regulatory subunits of NMDAR in several functions, here we will focus on the synaptic pool of NMDARs containing the GluN2A subunit, addressing its role in both physiology and pathological synaptic plasticity as well as the contribution in these events of different types of GluN2A-interacting proteins.
Highlights
N-Methyl-d-Aspartate Receptors (NMDARs) are ligand- and voltage-gated ionotropic glutamate receptors promoting Ca2+ and Na+ influx
The influence of the NMDAR subunit composition on synaptic plasticity has been subject of a vast number of studies, trying to explain the unsolved question on how different patterns of neuronal stimulation lead to opposite modulation of synaptic strength acting on the same type of receptor
NMDARs have been intensively studied in the last decades because of their involvement in many aspects of neuronal transmission as well as learning and memory
Summary
N-Methyl-d-Aspartate Receptors (NMDARs) are ligand- and voltage-gated ionotropic glutamate receptors (iGluRs) promoting Ca2+ and Na+ influx. In the canonical view, activation of NMDARs represents a coincidence detector of presynaptic glutamate release and postsynaptic depolarization [1,2]. Chen et al reported that GluN2A-containing NMDAR mediate large currents, as suggested by the peak current densities [27] This subunit grants the NMDAR a high channel open probability [27]. GluN2 subunits are the main regulators of the open/close state of the NMDAR In this context, GluN2A-containing receptors have a reversible calcium-dependent inactivation, whereas other kinds of NMDARs, like the GluN2B-containing ones, do not significantly suffer for calcium-dependent inactivation [29]. GluN2A confers to NMDAR specific electrophysiological properties, like high channel opening probability and conductance, more predisposed to desensitize but with a faster recovery, making these receptors versatile modulators of synaptic activity. We will focus on synaptic GluN2A-containing NMDARs, their role in synaptic plasticity and their contribution to pathological plasticity as observed in several brain disorders
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