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Also, a heightened phosphorylation level of GluA1 at serine 845 by FR-induced LTP instead of glycine-induced LTP was dependent on the activation of GluN2B, that will be supported by the outcomes from GluN2B antagonists, little interfering peptide and CRISPR-Cas9-mediated knock out of GluN2B. Taken together, we expose the significant role of GluN2B in FR-induced LTP, uncovering the role of GluN2B subunit of NMDA receptor in a specified cLTP. In t
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