Geon Anchoring of Calcineurin to GluN2B
Differentiates Its Contributions to LTD from GluN2A
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Abstract

GluN2A and GluN2B are the major subunits of NMDA receptors (NMDARs). It has been well documented that GluN2A and GluN2B contribute differentially to NMDAR-dependent long-term potentiation (LTP) and long-term depression (LTD). This paper shows that the key factor is the association of calcineurin with GluN2B, not GluN2A, via the A-kinase anchoring protein (AKAP79 in humans or AKAP150 in rodents). This fact explains why the brief tetanic stimulation induces LTP whereas the prolonged low frequency stimulation produces LTD. The paper also contrasts the calcineurin-mediated LTD with recently discovered CaMKII-mediated LTD, which is induced by prolonged agonist binding to NMDARs, but does not require Ca2+ influx through NMDARs.

 

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