CaMKII binding to GluN2B is important for massed spatial learning in the Morris water maze.

ABSTRACT: Learning and memory as well as long-term potentiation (LTP) depend on Ca (2+) influx through the NMDA-type glutamate receptor (NMDAR) and the resulting activation of the Ca (2+) and calmodulin-dependent protein kinase (CaMKII). Ca (2+) influx via the NMDAR triggers CaMKII binding to the NMDAR for enhanced CaMKII accumulation at post-synaptic sites that experience heightened activity as occurring during LTP. Previously, we generated knock-in (KI) mice in which we replaced two residues in the NMDAR GluN2B subunit to impair CaMKII binding to GluN2B. Various forms of LTP at the Schaffer collateral synapses in CA1 are reduced by 50%. Nevertheless, working memory in the win-shift 8 arm maze and learning of the Morris water maze (MWM) task was normal in the KI mice although recall of the task was

SUBMITTER: Stein IS 

PROVIDER: S-EPMC4149248 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature