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Science 16 December 1994:
Vol. 266. no. 5192, pp. 1881 - 1885
DOI: 10.1126/science.7997883
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Articles

Science, Vol 266, Issue 5192, 1881-1885
Copyright © 1994 by American Association for the Advancement of Science

articles

Potentiated transmission and prevention of further LTP by increased CaMKII activity in postsynaptic hippocampal slice neurons

DL Pettit, S Perlman, and R Malinow

Neuroscience Program, University of Iowa, Iowa City 52242.

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.


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