A Computational Model of Bidirectional Plasticity Regulation by betaCaMKII (Pinto et al. 2019)

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We present a computational model that suggests how calcium-calmodulin dependent protein kinase II can act as a molecular switch in synaptic plasticity induction at an important cerebellar synapse (between parallel fibres and Purkinje cells). Our simulation results provide a potential explanation for experimental data by van Woerden et al (Van Woerden G, Hoebeek F, Gao Z, Nagaraja R, Hoogenraad C, Kushner S, et al. [beta]CaMKII controls the direction of plasticity at parallel fiber-Purkinje cell synapses. Nat Neurosci. 2009;12(7):823-825). These experiments were performed in the lab led by Professor Chris De Zeeuw.
1 . Pinto TM, Schilstra MJ, Roque AC, Steuber V (2019) Binding of Filamentous Actin to CaMKII as a Potential Mechanism for the Regulation of Bidirectional Synaptic Plasticity by ├čCaMKII in Cerebellar Purkinje Cells PLOS Computational Biology, accepted
Model Information (Click on a link to find other models with that property)
Model Type: Synapse;
Brain Region(s)/Organism: Cerebellum;
Cell Type(s):
Gap Junctions:
Receptor(s): AMPA;
Simulation Environment: XPP;
Model Concept(s): Long-term Synaptic Plasticity; Synaptic Plasticity; Calcium dynamics; Depression;
Search NeuronDB for information about:  AMPA;
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