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Ca2+buffering as a mechanism of short-term synaptic plasticity

BMC Neuroscience201314 (Suppl 1) :P269

https://doi.org/10.1186/1471-2202-14-S1-P269

  • Published:

Keywords

  • Synaptic Transmission
  • Buffer Reaction
  • Deep Insight
  • Endocrine Cell
  • Cell Process
Spatio-temporal compartmentalization allows Ca2+ signals to simultaneously regulate multiple vital cell processes and relies in part on Ca2+ buffers that absorb at least 98% of Ca2+ ions entering the cytoplasm. Computational modeling has played a central role in the understanding of localized Ca2+ signals in neurons and other cell types. Although many models consider only simple, one-to-one Ca2+ buffering stoichiometry, practically all buffers have multiple Ca2+ binding sites which often display cooperative binding (e.g., calretinin [13], calmodulin [4, 5] ). Given the simplest case of two binding sites, cooperativity manifests itself in an order of magnitude difference in the binding and/or unbinding rates of the two consecutive Ca2+ binding steps in the following buffer reaction:
Here we extend recent modeling studies of cooperative buffering [15], and find that it can lead to spatio-temporal Ca2+ signals that cannot be achieved by any combination of non-cooperative buffers, in particular during a sequence of action potentials or synaptic inputs. Namely, Figure 1B shows that cooperative Ca2+ buffering can potentially serve as a mechanism of short-term synaptic depression, in contrast to the case of non-cooperative buffers (Figure 1A), which are believed to underlie short-term synaptic facilitation in certain types of mammalian synapses [6, 7].
Figure 1
Figure 1

[Ca 2+ ] elevation during a 40 Hz train of 1ms-long Ca 2+ pulses at 100nm from the Ca 2+ source. A: In the presence of a non-cooperative buffer, Ca2+ transients facilitate due to gradual depletion (saturation) of free buffer [6, 7]. B: In the presence of a cooperative buffer, Ca2+ transients depress as a result of increasing exposure of the high-affinity Ca2+ binding site. Both simulations done in 1D geometry (0.5 μm axonal segment), computed using CalC version 7.2 (http://www.calciumcalculator.org)

We explore this phenomenon in detail, demonstrating the dependence of such buffer-induced short-term synaptic plasticity on all relevant buffering parameters. These results may lead to better understanding of post-synaptic Ca2+ dynamics as well, yielding a deeper insight into synaptic transmission and its dynamic regulation, and may also have relevance for Ca2+-dependent processes in other cells such as endocrine cells, myocytes and immune system cells.

Declarations

Acknowledgements

This work was supported in part by NSF grant DMS-0817703.

Authors’ Affiliations

(1)
Department of Mathematical Sciences, New Jersey Institute of Technology, Newark, NJ 07102, USA

References

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Copyright

© Matveev; licensee BioMed Central Ltd. 2013

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/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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