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The discovery of a requirement for N-methyl d-aspartate receptor (NMDAR) activation in long-term potentiation (LTP) set off an explosion of interest in the mechanisms of NMDAR-dependent synaptic plasticity. Meanwhile other research has advanced our understanding of how NMDAR activation regulates neuronal death and survival. Surprisingly, there have been few attempts to correlate these important areas...
Synaptic plasticity mediated by NMDA glutamate receptors is thought to be a primary mechanism underlying the formation of new memories. Activation of GluN2A NMDA receptor subunits may induce long-term potentiation (LTP), whereas low-frequency stimulation of GluN2B receptors induces long-term depression (LTD). In the present study, we show that blockade of GluN2A, but not GluN2B receptors with NVP-AAM077...
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