receptors and contribute to synaptic plasticity and LTP.234 Mutation of the αCaMKII autophosphorylation site Thr-286 abolishes stimulus-evoked LTP in rat hippocampal slices and results in spatial memory deficits in the mutant mice.234 In rat hippocampal cultures, the dopamine D1 agonist SKF 81297 increases GluR1 trafficking to the cell surface, which is partially attenuated by the CaMKII inhibitor KN-62.79 Thus CaMKII plays an important role in synaptic plasticity.
