Abstract
NMDA ionotropic glutamate receptors (NMDARs) are crucial in activity-dependent synaptic changes and in learning and memory. NMDARs are composed of two GluN1 essential subunits and two regulatory subunits which define their pharmacological and physiological profile. In CNS structures involved in cognitive functions as the hippocampus and prefrontal cortex, GluN2A and GluN2B are major regulatory subunits; their expression is dynamic and tightly regulated, but little is known about specific changes after plasticity induction or memory acquisition. Data strongly suggest that following appropriate stimulation, there is a rapid increase in surface GluN2A-NMDAR at the postsynapses, attributed to lateral receptor mobilization from adjacent locations. Whenever synaptic plasticity is induced or memory is consolidated, more GluN2A-NMDARs are assembled likely using GluN2A from a local translation and GluN1 from local ER. Later on, NMDARs are mobilized from other pools, and there are de novo syntheses at the neuron soma. Changes in GluN1 or NMDAR levels induced by synaptic plasticity and by spatial memory formation seem to occur in different waves of NMDAR transport/expression/degradation, with a net increase at the postsynaptic side and a rise in expression at both the spine and neuronal soma. This review aims to put together that information and the proposed hypotheses.
Highlights
Learning and memory, as well as synaptic plasticity which is considered their electrophysiological correlate, depend on glutamatergic transmission
NMDA ionotropic glutamate receptors (NMDARs) are composed of 2 GluN1 obligatory subunits encoded by one gene, with eight variants originated by alternative splicing [7, 8], and 2 regulatory subunits that contain the glutamate binding site
Those regulatory subunits are encoded by different genes; there are four GluN2 subunits (GluN2A–D), which are codified by four different genes, and two GluN3 subunits (GluN3A and B), which are codified by two different genes [5, 9]
Summary
As well as synaptic plasticity which is considered their electrophysiological correlate, depend on glutamatergic transmission (reviewed in [1]). NMDARs are composed of 2 GluN1 obligatory subunits encoded by one gene, with eight variants originated by alternative splicing [7, 8], and 2 regulatory subunits that contain the glutamate binding site. Those regulatory subunits are encoded by different genes; there are four GluN2 subunits (GluN2A–D), which are codified by four different genes, and two GluN3 subunits (GluN3A and B), which are codified by two different genes [5, 9]. In CNS regions involved in cognitive functions, like the hippocampus and prefrontal cortex (PFC), GluN2A and GluN2B are the major regulatory subunits [5, 13]. This review aims to put together that information and the proposed hypotheses on those changes
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
