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Calcium-calmodulin-dependent protein kinase II (CaMKII) is a necessary component of the cellular machinery underlying learning and memory. Here, a constitutively active form of this enzyme, CaMKII(1-290), was introduced into neurons of hippocampal slices with a recombinant vaccinia virus to test the hypothesis that increased postsynaptic activity of this enzyme is sufficient to produce long-term synaptic potentiation (LTP), a prominent cellular model of learning and memory. Postsynaptic expression of CaMKII(1-290) increased CaMKII activity, enhanced synaptic transmission, and prevented more potentiation by an LTP-inducing protocol. These results, together with previous studies, suggest that postsynaptic CaMKII activity is necessary and sufficient to generate LTP.
Pettit et al. (1994) studied this question.