Email updates

Keep up to date with the latest news and content from BMC Neuroscience and BioMed Central.

This article is part of the supplement: Nineteenth Annual Computational Neuroscience Meeting: CNS*2010

Open Access Open Badges Poster Presentation

Modeling signal transduction in synaptic plasticity: comparison of models and methods

Tiina Manninen*, Katri Hituri, Eeva Toivari and Marja-Leena Linne

Author Affiliations

Department of Signal Processing, Tampere University of Technology, P.O. Box 553, FI-33101 Tampere, Finland

For all author emails, please log on.

BMC Neuroscience 2010, 11(Suppl 1):P190  doi:10.1186/1471-2202-11-S1-P190

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

Published:20 July 2010

© 2010 Manninen et al; licensee BioMed Central Ltd.

Poster Presentation

Long-term activity-dependent strengthening (LTP) and weakening (LTD) of synapses are two forms of synaptic plasticity. Both LTP and LTD participate in storing information and inducing processes that ultimately lead to learning and memory (e.g., [1]). Several mechanisms have been shown to be the reason for changes in synaptic strength, for example changes in neurotransmitter release, conductivity of receptors, numbers of receptors, numbers of active synapses, and structure of synapses [2]. At present, there are more than hundred molecules found important in LTP and LTD.

Several computational models, simple and more complex ones, have been developed to describe the mechanisms behind synaptic plasticity at the biochemical level. Simplest models have only one reversible reaction and most complicated ones have several hundred reactions.

In this study, we evaluate different computational models for describing LTP and LTD phenomena. Selected models, including both simplified (e.g., [3,4]) and biophysically more detailed (e.g., [5,6]) ones, are implemented, and their behavior is simulated with well-established deterministic and stochastic approaches [7]. Especially, we concentrate on the input-output relationship in simulations of the models. When using the same input, many of the models are found to give different responses. One of the reasons is that some of the models studied can mimic both the induction and maintenance of synaptic plasticity, whereas others are found to explain only the induction. Furthermore, the role of some specific molecules important in LTP and LTD is studied. Even thought the simplest models do not take into account all the details in biological knowledge, they can be used to predict different events, which is very important when modeling synaptic plasticity. The ultimate goal of this work is to provide realistic, yet simple enough models for describing LTP and LTD phenomena and addressing the general principles of information storage in neurons.


This study was supported by the Academy of Finland, application numbers 129657 (Finnish Programme for Centres of Excellence in Research 2006-2011), 126556, and 137349, as well as the Finnish Foundation for Economic and Technology Sciences - KAUTE, Emil Aaltonen Foundation, Tampere University of Technology Graduate School, and Tampere Graduate School in Information Science and Engineering.


  1. Citri A, Malenka RC: Synaptic plasticity: multiple forms, functions, and mechanisms.

    Neuropsychopharmacology 2008, 33(1):18-41. PubMed Abstract | Publisher Full Text OpenURL

  2. Hayer A, Bhalla US: Molecular switches at the synapse emerge from receptor and kinase traffic.

    PLoS Comput Biol 2005, 1(2):137-154. PubMed Abstract | Publisher Full Text | PubMed Central Full Text OpenURL

  3. Delord B, Berry H, Guigon E, Genet S: A new principle for information storage in an enzymatic pathway model.

    PLoS Comput Biol 2007, 3(6):e124. PubMed Abstract | Publisher Full Text | PubMed Central Full Text OpenURL

  4. 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(49):13132-13138. PubMed Abstract | Publisher Full Text | PubMed Central Full Text OpenURL

  5. Lindskog M, Kim M, Wikström MA, Blackwell KT, Hellgren Kotaleski J: Transient calcium and dopamine increase PKA activity and DARPP-32 phosphorylation.

    PLoS Comput Biol 2006, 2(9):e119. PubMed Abstract | Publisher Full Text | PubMed Central Full Text OpenURL

  6. Graupner M, Brunel N: STDP in a bistable synapse model based on CaMKII and associated signaling pathways.

    PLoS Comput Biol 2007, 3(11):e221. PubMed Abstract | Publisher Full Text | PubMed Central Full Text OpenURL

  7. Manninen T, Linne ML, Ruohonen K: Developing Itô stochastic differential equation models for neuronal signal transduction pathways.

    Comput Biol Chem 2006, 30(4):280-291. PubMed Abstract | Publisher Full Text OpenURL