Abstract
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.
MeSH terms
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2-Amino-5-phosphonovalerate / pharmacology
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Animals
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Calcium-Calmodulin-Dependent Protein Kinase Type 2
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Calcium-Calmodulin-Dependent Protein Kinases / metabolism*
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Cell Line
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Genetic Vectors
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Hippocampus / cytology
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Hippocampus / enzymology
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Hippocampus / physiology*
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In Vitro Techniques
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Long-Term Potentiation / drug effects
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Long-Term Potentiation / physiology*
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Membrane Potentials
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Patch-Clamp Techniques
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Pyramidal Cells / enzymology
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Pyramidal Cells / physiology*
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Rats
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Recombinant Proteins / metabolism
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Synaptic Transmission / drug effects
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Synaptic Transmission / physiology*
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Transfection
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Vaccinia virus / genetics
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Vaccinia virus / physiology
Substances
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Recombinant Proteins
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2-Amino-5-phosphonovalerate
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Calcium-Calmodulin-Dependent Protein Kinase Type 2
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Calcium-Calmodulin-Dependent Protein Kinases