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.
Original language | English |
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Title of host publication | International Conference of Computational Methods in Sciences and Engineering 2015, ICCMSE 2015 |
Publisher | American Institute of Physics (AIP) |
Volume | 1702 |
ISBN (Electronic) | 9780735413498 |
DOIs | |
Publication status | Published - 31 Dec 2015 |
Event | International Conference of Computational Methods in Sciences and Engineering 2015, ICCMSE 2015 - Athens, Greece Duration: 20 Mar 2015 → 23 Mar 2015 |
Conference
Conference | International Conference of Computational Methods in Sciences and Engineering 2015, ICCMSE 2015 |
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Country/Territory | Greece |
City | Athens |
Period | 20/03/15 → 23/03/15 |
Keywords
- calcium
- calmodulin
- cerebellum
- learning
- long-term depression
- long-term potentiation
- memory
- simulation