University of Hertfordshire

Unravelling how βCaMKII controls the direction of plasticity at parallel fibre-Purkinje cell synapses

Research output: Chapter in Book/Report/Conference proceedingConference contribution

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Original languageEnglish
Title of host publicationInternational Conference of Computational Methods in Sciences and Engineering 2015, ICCMSE 2015
PublisherAmerican Institute of Physics Inc.
Volume1702
ISBN (Electronic)9780735413498
DOIs
StatePublished - 31 Dec 2015
EventInternational Conference of Computational Methods in Sciences and Engineering 2015, ICCMSE 2015 - Athens, Greece

Conference

ConferenceInternational Conference of Computational Methods in Sciences and Engineering 2015, ICCMSE 2015
CountryGreece
CityAthens
Period20/03/1523/03/15

Abstract

Long-term plasticity at parallel fibre (PF)-Purkinje cell (PC) synapses is thought to mediate cerebellar motor learning. It is known that calcium-calmodulin dependent protein kinase II (CaMKII) is essential for plasticity in the cerebellum. Recently, Van Woerden et al. demonstrated that the β isoform of CaMKII regulates the bidirectional inversion of PF-PC plasticity. Because the cellular events that underlie these experimental findings are still poorly understood, our work aims at unravelling how βCaMKII controls the direction of plasticity at PF-PC synapses. We developed a bidirectional plasticity model that replicates the experimental observations by Van Woerden et al. Simulation results obtained from this model indicate the mechanisms that underlie the bidirectional inversion of cerebellar plasticity. As suggested by Van Woerden et al., the filamentous actin binding enables βCaMKII to regulate the bidirectional plasticity at PF-PC synapses. Our model suggests that the reversal of long-term plasticity in PCs is based on a combination of mechanisms that occur at different calcium concentrations.

ID: 11333430