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.

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Keywords Animals, Calcineurin/metabolism, Calcium-Calmodulin-Dependent Protein Kinase Type 2/genetics/*metabolism, Cyclosporine/pharmacology, Electric Stimulation, Enzyme Inhibitors/pharmacology, Long-Term Potentiation/physiology, Long-Term Synaptic Depression/drug effects/physiology, Mice, Mice, Knockout, Models, Neurological, Neuronal Plasticity/*physiology, Patch-Clamp Techniques, Purkinje Cells/*physiolog, Synapses/*physiology
Persistent URL dx.doi.org/10.1038/nn.2329, hdl.handle.net/1765/22574
Citation
van Woerden, G.M., Hoebeek, F.E., Gao, Z., Nagaraja, R.Y., Hoogenraad, C.C., Kushner, S.A., … Elgersma, Y.. (2009). betaCaMKII controls the direction of plasticity at parallel fiber–Purkinje cell synapses. Nature Neuroscience, 12(7), 823–825. doi:10.1038/nn.2329