Skip to main content

Model for the induction of spike timing-dependent plasticity by pre- and postsynaptic spike trains

Spike timing-dependent plasticity (STDP), a process in which changes in synaptic strength are determined by the relative timing of pre- and postsynaptic activity, has been studied and modeled by a number of researchers, but many questions still remain. It has been suggested that STDP involves a postsynaptic chemical network with stable states corresponding to long term potentiation (LTP) and long term depression (LTD). It is believed that the switching between these states is driven by the postsynaptic Ca2+ concentration, but the manner in which the Ca2+ dynamics is able to trigger either LTP or LTD, depending on the relative timing of pre- and postsynaptic activity remains unclear.

We have investigated a model of STDP that combines (1) the tristable chemical network involving CaMKII and PP2A studied by Pi and Lisman [1], with (2) compartmental modeling of backpropagating action potentials (BPAPs), N-methyl D-aspartate receptors (NMDARs), and voltage-dependent calcium channels (VDCCs). In previous work we have studied how this model responds when a presynaptic pulse arrives either shortly before or shortly after a postsynaptic pulse (a BPAP), and shown how this model leads naturally to LTP when the presynaptic pulse arrives first, or LTD when the postsynaptic pulse arrives first, in agreement as found in experimental studies (e.g., [2] and [3]). The response to spike triplets and other more complex pre- and postsynaptic spike trains are also of interest. Experiments [4] have shown that the response to such multispike trains is not simply the sum of the responses to the component spike pairs. For example, the response to a spike triplet consisting of pre-post-presynaptic spikes is often not explained by the simple addition of the responses to a pre-post spike pair followed by a post-pre spike pair. Previous work has proposed only heuristic rules for such multispike responses. In this paper we describe the application of our model of STDP to multispike situations. Our model exhibits a non-additive response similar to that observed by Wang et al. [4], and gives insight into how this non-additivity arises from properties of the CaMKII/PP2A network.


  1. Pi HJ, Lisman JE: Coupled Phosphatase and Kinase Switches Produce the Tristability Required for Long-Term Potentiation and Long-Term Depression. J Neurosci. 2008, 28: 13132-13138. 10.1523/JNEUROSCI.2348-08.2008.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  2. Bi GQ, Poo MM: Synaptic Modifications in Cultured Hippocampal Neurons: Dependence on Spike Timing, Synaptic Strength, and Postsynaptic Cell Type. J Neurosci. 1998, 18: 10464-10472.

    CAS  PubMed  Google Scholar 

  3. Markram H, Lubke J, Frotscher M, Sakmann B: Regulation of Synaptic Efficacy by Coincidence of Postsynaptic APs and EPSPs. Science. 1997, 275: 213-215. 10.1126/science.275.5297.213.

    Article  CAS  PubMed  Google Scholar 

  4. Wang HX, Gerkin RC, Nauen DW, Bi GQ: Coactivation and Timing-Dependent Integration of Synaptic Potentiation and Depression. Nat Neurosci. 2005, 8: 187-193. 10.1038/nn1387.

    Article  CAS  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations


Corresponding author

Correspondence to Kristofor D Carlson.

Rights and permissions

Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution 2.0 International License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Reprints and Permissions

About this article

Cite this article

Carlson, K.D., Giordano, N. Model for the induction of spike timing-dependent plasticity by pre- and postsynaptic spike trains. BMC Neurosci 11 (Suppl 1), P188 (2010).

Download citation

  • Published:

  • DOI: