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Memory and the NMDA receptors - PubMed

  • ️Thu Jan 01 2009

Memory and the NMDA receptors

Fei Li et al. N Engl J Med. 2009.

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Conflict of interest statement

No potential conflict of interest relevant to this article was reported.

Figures

Figure 1
Figure 1. Neuron Showing Glutamate Receptors and Synaptic Plasticity

Various experiments suggest that memory formation involves two types of glutamate receptors: the N-methyl-D-aspartate receptor (NMDAR) and the α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR). These receptors sit on the surface of postsynaptic neurons. AMPARs allow sodium to flow into the postsynaptic cell, resulting in depolarization. NMDARs are permeable to both ionic sodium and calcium. The subsequent influx of ionic calcium into the postsynaptic terminals through the NMDAR activates biochemical cascades that trigger the up-regulation of AMPARs to the membrane while increasing the AMPAR’s sensitivity to glutamate and thus strengthen the synapses. A recent study by Ng et al. showed that the deletion of Neto1, a postsynaptic protein associated with the NMDAR complex, leads to deficits in both synaptic plasticity and cognition. Neto1 binds to PSD-95, a protein that is almost exclusively located in the postsynaptic density of neurons, and is important in anchoring synaptic proteins. Neto1 also binds to NR2A and NR2B, two isoforms of NR2 subunits that are essential for NMDAR functions. The composition of NR2A and NR2B in the NMDAR substantially modulates its channel properties. Stimulation of the AMPAR can partially compensate for deficits caused by Neto1 deletion.

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