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

Open Access Poster presentation

An efficient Ca2+ based plasticity rule with combined Ca2+ sources

Dominic Standage* and Thomas Trappenberg

Author Affiliations

Faculty of Computer Science, Dalhousie University, Halifax, Canada

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BMC Neuroscience 2007, 8(Suppl 2):P93  doi:10.1186/1471-2202-8-S2-P93


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


Published:6 July 2007

© 2007 Standage and Trappenberg; licensee BioMed Central Ltd.

Poster presentation

A number of research groups have proposed generative, Ca2+ based plasticity models in recent years. Such rules are based on the premise that moderate, above-basal levels of post-synaptic Ca2+ lead to long term depression (LTD) and that high levels lead to long term potentiation (LTP). We present such a rule and discuss its assumptions and implications.

Our rule has similarities with two models in [1] in that Ca2+ may enter the post-synaptic density (PSD) through voltage gated channels Ca2+(V) and NMDA receptor (NMDAR) mediated channels Ca2+(V, NMDA). Unlike Model 1 in their study and the model of the Shouval group [2], our model achieves spike time dependent LTD without the requirement that back-propagating action potentials (BAP's) have a long tail. Thus, we do not assume this tail is sufficient to expel Mg2+ from glutamate-bound NMDAR's. In our model, LTP and LTD processes are compounded while Ca2+ exceeds LTP and LTD thresholds respectively. We do not use a specific function of peak Ca2+ or the time-integral of pre- and post-synaptic interactions.

The simple formulation of our model makes fewer assumptions about the underlying biology of NMDAR-dependent plasticity than the models in [1] and [2], but our simulations of spike-time dependent plasticity (STDP) experiments show similar output to theirs. For post-before-pre spike pairings, depression is graded because the respective time courses of Ca2+ and NMDAR-activation are sufficiently long to interact with one another. Ca2+(V) is spatially non-specific because it is driven by the BAP, but NMDAR's provide an indicator of pre-synaptic plasticity that interacts with this Ca2+ source. We use NMDAR's in this role for convenience, as other molecules could serve this purpose. This mechanism is similar to Model 2 in [1] where the two Ca2+ sources are separate. Here, the Ca2+ sources are combined to exceed the LTP threshold, resulting in the much-debated LTD window at long-latency pre-before-post pairings.

Our model points to several mechanisms for experimental study. For instance, spatially non-specific Ca2+(V) must integrate with Ca2+(V, NMDA) in the PSD very quickly to produce LTP. Alternatives to rapid integration at the PSD include the possibility that plasticity-inducing processes determine the relative levels of Ca2+ inside and outside the PSD, that Ca2+(V, NMDA) exceeds Ca2+(V) by some margin, or that Ca2+-dependent release from internal stores plays a role in this regard.

References

  1. Karmarkar U, Buonomano D: A model of spike-timing dependent plasticity: one or two coincidence detectors?

    J Neurophysiol 2002, 88:507-513. PubMed Abstract | Publisher Full Text OpenURL

  2. Shouval H, Bear M, Cooper L: A unified model of NMDA receptor-dependent bidirectional synaptic plasticity.

    PNAS 2002, 99:10831-10836. PubMed Abstract | Publisher Full Text | PubMed Central Full Text OpenURL