Abstract
We found that betaCaMKII, the predominant CaMKII isoform of the cerebellum, is important for controlling the direction of plasticity at the parallel fiber-Purkinje cell synapse; a protocol that induced synaptic depression in wild-type mice resulted in synaptic potentiation in Camk2b knockout mice and vice versa. These findings provide us with unique experimental insight into the mechanisms that transduce graded calcium signals into either synaptic depression or potentiation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Calcineurin / metabolism
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Calcium-Calmodulin-Dependent Protein Kinase Type 2 / genetics
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Calcium-Calmodulin-Dependent Protein Kinase Type 2 / metabolism*
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Cyclosporine / pharmacology
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Electric Stimulation
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Enzyme Inhibitors / pharmacology
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In Vitro Techniques
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Long-Term Potentiation / physiology
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Long-Term Synaptic Depression / drug effects
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Long-Term Synaptic Depression / physiology
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Mice
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Mice, Knockout
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Models, Neurological
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Neuronal Plasticity / physiology*
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Patch-Clamp Techniques
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Purkinje Cells / physiology*
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Synapses / physiology*
Substances
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Enzyme Inhibitors
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Cyclosporine
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Calcium-Calmodulin-Dependent Protein Kinase Type 2
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Camk2b protein, mouse
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Calcineurin