Biochemical regulation of the CaMKII/GluN2B interaction and its role in the maintenance of synaptic strength
Ca²⁺/Calmodulin (CaM)-dependent protein kinase II (CaMKII) is a major regulator of long-term potentiation (LTP) in the hippocampus. During this process, CaMKII becomes activated and translocates to the activated synapse through an interaction with the GluN2B subunit of the NMDAR. This interaction persists after the initial stimulus has subsided and has therefore been proposed to act as a form of molecular memory. For this reason, the mechanisms that underlie the interaction and the physiological functions related to its induction and persistence are of great interest. It was first shown here ...
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