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1 Department of Physiology and Biophysics, University of Iowa, Iowa City, Iowa 52242; and 2 Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724
Shirke, Aneil M. and Roberto Malinow. Mechanisms of potentiation by calcium-calmodulin kinase II of postsynaptic sensitivity in rat hippocampal CA1 neurons. J. Neurophysiol. 78: 2682-2692, 1997. Preactivated recombinant 
-calcium-calmodulin dependent multifunctional protein kinase II (CaMKII*) was perfused internally into CA1 hippocampal slice neurons to test the effect on synaptic transmission and responses to exogenous application of glutamate analogues. After measurement of baseline transmission, internal perfusion of CaMKII* increased synaptic strength in rat hippocampal neurons and diminished the fraction of synaptic failures. After measurement of baseline responses to applied transmitter, CaMKII* perfusion potentiated responses to kainate but not responses to N-methyl-D-aspartate. Internal perfusion of CaMKII*potentiated the maximal effect of kainate. Potentiation byCaMKII* did not change the time course of responses to kainate, whereas increasing response size by pharmacologically manipulating desensitization or deactivation rate constants significantly altered the time course of responses. Nonstationary fluctuation analysis of responses to kainate showed a decrease in the coefficient of variation after potentiation by CaMKII*. These data support the hypothesis that CaMKII increases postsynaptic responsiveness by increasing the available number of active -amino-3-hydroxy-5-methylisoxazole-4-propionic acid/kainate channels and suggests that a similar process may occur during the expression of long-term potentiation.
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