Advertisement

BMC Neuroscience

, 16:P268 | Cite as

A spatiotemporal model of spine calcium dynamics in the hippocampus

  • Thom Griffith
  • Jack Mellor
  • Krasi Tsaneva-Atanasova
Poster presentation
  • 230 Downloads

Keywords

Finite Element Method Spatial Variation Signalling Cascade Synaptic Plasticity Biological Role 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Ca2+-signalling in dendritic spines is required for NMDA receptor-dependent synaptic plasticity at glutamatergic synapses in the hippocampus [1]. However, it is not clear whether plasticity induction is dependent solely on the global signal, i.e., the spine volume-averaged Ca2+ signal; or whether plasticity induction is also sensitive to Ca2+-channel nanodomain signaling [2]. A working hypothesis of this work is that temporal and spatial variations in postsynaptic intracellular [Ca2+]-fields may be significant factors governing the signalling cascades that lead to either long-term synaptic potentiation or depression. Direct measurement of [Ca2+] distributions in dendritic spines is experimentally difficult but we can investigate this hypothesis using mathematical models of Ca2+ diffusion.

We have developed a spatio-temporal model of Ca2+ diffusion in three dimensions. We then study our model using finite element methods. The model allows predictions of intracellular [Ca2+]-field responses to combinations of pre- and post-synaptic spikes with nanometre and millisecond spatio-temporal resolution. Our results so far indicate that Ca2+ signalling is highly spatially non-uniform and that Ca2+ signal differences between induction protocols is dependent on location within the spine. This has implications for the ultimate biological role of the Ca2+ signal given that the relevant receptors in the spine are organised inhomogeneously [3].

Notes

Acknowledgements

Support for this work was provided by the EPSRC, UK (EP/I013717/1).

References

  1. 1.
    Malenka RC, Bear MF: LTP and LTD: an embarrassment of riches. Neuron. 2004, 44 (1): 5-21.PubMedCrossRefGoogle Scholar
  2. 2.
    Chen Y, Sabatini BL: Signaling in dendritic spines and spine microdomains. Current Opinion in Neurobiology. 2012, 22 (3): 389-396.PubMedPubMedCentralCrossRefGoogle Scholar
  3. 3.
    Mori MX, Erickson MG, Yue DT: Functional stoichiometry and local enrichment of calmodulin interacting with Ca2+ channels. Science. 2004, 304 (5669): 432-435.PubMedCrossRefGoogle Scholar

Copyright information

© Griffith et al. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors and Affiliations

  • Thom Griffith
    • 1
  • Jack Mellor
    • 2
  • Krasi Tsaneva-Atanasova
    • 3
  1. 1.Department of Engineering MathsUniversity of BristolBristolUK
  2. 2.School of Physiology and PharmacologyUniversity of BristolBristolUK
  3. 3.Department of MathematicsUniversity of ExeterExeterUK

Personalised recommendations