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Illustration shows the mechanism of LTP and LTD. Normally, the NMDA receptor in the postsynaptic neuron is activated by glutamate binding, but only after depolarization removes an inhibitory magnesium ion. Once the magnesium is removed, calcium can enter the cell. In response to an increase in intracellular calcium, AMPA receptors are inserted into the plasma membrane, which amplifies the signal resulting in LTP. LDP occurs when low-frequency stimulation results in the activation of a…


Wind-up pain is caused by activation of normally dormant NMDA receptors.Activated NMDA receptors cause - influx of Calcium into Dorsal Horn Wide Dynamic Range interneurons resulting in a cycle of - increased production/sensitization/number of NMDA receptors & increased release of Glutamate/Substance-P at presynaptic sites This positive feedback loop results in a marked increase in the pain signal ultimately perceived by the brain.

What is Anti-NMDA Receptor Encephalitis? (In English, French & Spanish) - The Anti NMDA Receptor Encephalitis Foundation Inc. The Anti NMDA Receptor Encephalitis Foundation Inc.


Deep dive into NMDA receptor variation and link to epilepsy, ID Check more at

Research Gives Unprecedented 3D View of Important Brain Receptor - X-ray crystal structure of the NMDA receptor showing its mushroom- like shape, with receptor subunits in different colors. Credit Oregon Health and Science University.


"Anti-NMDA (N-methyl D-aspartate) receptor encephalitis is an acute form of encephalitis, potentially lethal but with high probability for recovery, caused by autoimmune reaction against NR1- and NR2-subunits of the glutamate NMDA receptor. Different descriptions and syndromal designations for this disease existed in the medical literature prior to 2007, when the cause was established and it received its current name."