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This article is part of the supplement: Sixteenth Annual Computational Neuroscience Meeting: CNS*2007

Open Access Oral presentation

Activity-homeostasis preserves synaptic plasticity in Purkinje cell but calcium is not the activity-sensor

Pablo Achard1* and Erik De Schutter12

Author Affiliations

1 Theoretical Neurobiology, University of Antwerp, Belgium

2 Computational Neuroscience Unit, Okinawa Institute of Science and Technology, Onna-Son, Japan

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BMC Neuroscience 2007, 8(Suppl 2):S19  doi:10.1186/1471-2202-8-S2-S19


The electronic version of this article is the complete one and can be found online at:


Published:6 July 2007

© 2007 Achard and De Schutter; licensee BioMed Central Ltd.

Oral presentation

Activity homeostasis designates bio-mechanisms that regulate the activity of a neuron through the dynamic expression of ion channels or synapses [1]. We have recently shown [2] that it is possible to reproduce the complex activity of a Purkinje cell (PC) with very different combinations of ionic channel maximum conductances. However, if the global effect of homeostasis is starting to be understood, the detail of its machinery remains unknown. Some models [3,4] have hypothesized that one such mechanism could work via the regulation of the average cytoplasmic calcium concentration. While this hypothesis is attractive for rhythm generating neurons, it raises many questions for PCs since in these neurons calcium is supposed to play a very important role in long-term memory [5]. To address this question, we generate 81 PC models, all having a similar electrophysiological activity and all different enough from each other in their conductance set. We demonstrate that, while the somatic membrane voltage is stable during complex spikes, the somatic calcium behavior is very variable from cell to cell, in agreement with experimental results [6]. Therefore calcium is a weak candidate for being an activity-sensor in this cell. Conversely, we show that the calcium signal in the spiny dendrites is very robust. To further test whether long-term depression (LTD) mechanisms are preserved for these different models, we use a PC spine model of calcium signal transduction pathways [7]. In all our models, conjunctive parallel fibers-climbing fiber activation leads to a sustained calcium release from internal stores, hence LTD induction is preserved.

Acknowledgements

We thank T Doi, S Kuroda, T Michikawa, M Kawato and I Ogasawara for the availability of their model and the kind help they provided us to run it.

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