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

Standard

Unravelling how βCaMKII controls the direction of plasticity at parallel fibre-Purkinje cell synapses. / Pinto, Thiago M.; Schilstra, Maria J.; Steuber, Volker; Roque, Antonio C.

International Conference of Computational Methods in Sciences and Engineering 2015, ICCMSE 2015. Vol. 1702 American Institute of Physics Inc., 2015. 130002.

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

Harvard

Pinto, TM, Schilstra, MJ, Steuber, V & Roque, AC 2015, Unravelling how βCaMKII controls the direction of plasticity at parallel fibre-Purkinje cell synapses. in International Conference of Computational Methods in Sciences and Engineering 2015, ICCMSE 2015. vol. 1702, 130002, American Institute of Physics Inc., International Conference of Computational Methods in Sciences and Engineering 2015, ICCMSE 2015, Athens, Greece, 20-23 March. DOI: 10.1063/1.4938909

APA

Pinto, T. M., Schilstra, M. J., Steuber, V., & Roque, A. C. (2015). Unravelling how βCaMKII controls the direction of plasticity at parallel fibre-Purkinje cell synapses. In International Conference of Computational Methods in Sciences and Engineering 2015, ICCMSE 2015 (Vol. 1702). [130002] American Institute of Physics Inc.. DOI: 10.1063/1.4938909

Vancouver

Pinto TM, Schilstra MJ, Steuber V, Roque AC. Unravelling how βCaMKII controls the direction of plasticity at parallel fibre-Purkinje cell synapses. In International Conference of Computational Methods in Sciences and Engineering 2015, ICCMSE 2015. Vol. 1702. American Institute of Physics Inc.2015. 130002. Available from, DOI: 10.1063/1.4938909

Author

Pinto, Thiago M.; Schilstra, Maria J.; Steuber, Volker; Roque, Antonio C. / Unravelling how βCaMKII controls the direction of plasticity at parallel fibre-Purkinje cell synapses.

International Conference of Computational Methods in Sciences and Engineering 2015, ICCMSE 2015. Vol. 1702 American Institute of Physics Inc., 2015. 130002.

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

Bibtex

@inbook{e13046dd35754005b80521668995a24c,
title = "Unravelling how βCaMKII controls the direction of plasticity at parallel fibre-Purkinje cell synapses",
keywords = "calcium, calmodulin, cerebellum, learning, long-term depression, long-term potentiation, memory, simulation",
author = "Pinto, {Thiago M.} and Schilstra, {Maria J.} and Volker Steuber and Roque, {Antonio C.}",
year = "2015",
month = "12",
doi = "10.1063/1.4938909",
volume = "1702",
booktitle = "International Conference of Computational Methods in Sciences and Engineering 2015, ICCMSE 2015",
publisher = "American Institute of Physics Inc.",

}

RIS

TY - CHAP

T1 - Unravelling how βCaMKII controls the direction of plasticity at parallel fibre-Purkinje cell synapses

AU - Pinto,Thiago M.

AU - Schilstra,Maria J.

AU - Steuber,Volker

AU - Roque,Antonio C.

PY - 2015/12/31

Y1 - 2015/12/31

N2 - 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.

AB - 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.

KW - calcium

KW - calmodulin

KW - cerebellum

KW - learning

KW - long-term depression

KW - long-term potentiation

KW - memory

KW - simulation

UR - http://www.scopus.com/inward/record.url?scp=84984559308&partnerID=8YFLogxK

U2 - 10.1063/1.4938909

DO - 10.1063/1.4938909

M3 - Conference contribution

VL - 1702

BT - International Conference of Computational Methods in Sciences and Engineering 2015, ICCMSE 2015

PB - American Institute of Physics Inc.

ER -