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


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.

Model Type: Synapse

Region(s) or Organism(s): Cerebellum

Receptors: AMPA

Model Concept(s): Long-term Synaptic Plasticity; Synaptic Plasticity; Calcium dynamics; Depression

Simulation Environment: XPPAUT

References:

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.


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