Binding of CaMKII to the NMDA receptor is sufficient for long-term potentiation.

Learning and the underlying long-lasting increases in glutamatergic synapse strength [called long-term potentiation (LTP)] require both Ca 2+ influx through NMDA-type glutamate receptors (NMDARs) and the kinase CaMKII. New evidence now suggests that CaMKII can induce LTP purely by binding to the NMDAR subunit GluN2B and does not require the catalytic activity of the kinase.