Long-term potentiation (LTP) in the CA1 area of the hippocampus is considered to be a synaptic model for learning and memory. The induction of LTP is initiated by activation of the NMDA glutamate receptor in the postsynaptic membrane and a subsequent increase in Ca2+-influx into the neurons following glutamate release. The action of Ca2+ has been proposed to be mediated by Ca2+-dependent protein kinases. Recent studies indicate that, among the protein kinases, Ca2+/calmodulin-dependent protein kinase II is implicated in the induction of LTP in the hippocampus.