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: Eighteenth Annual Computational Neuroscience Meeting: CNS*2009

Open Access Poster presentation

A model for cortical remapping and structural plasticity following focal retinal lesions

Markus Butz12*, Florentin Wörgötter2 and Arjen van Ooyen1

Author Affiliations

1 Dept. for Integrative Neurophysiology, VU University, Amsterdam, 1081NL, The Netherlands

2 Bernstein Center for Computational Neuroscience, University of Göttingen, 37073 Göttingen, Germany

For all author emails, please log on.

BMC Neuroscience 2009, 10(Suppl 1):P206  doi:10.1186/1471-2202-10-S1-P206


The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1471-2202/10/S1/P206


Published:13 July 2009

© 2009 Butz et al; licensee BioMed Central Ltd.

Poster presentation

It is still debatable to what extent structural plasticity in terms of synaptic rewiring is the cause for lesion-induced or experience-dependent cortical remapping [1]. Recent two-photon laser imaging studies demonstrate that synaptic rewiring is persistent in the adult brain and is dramatically increased following brain lesions or after a loss of sensory input (deafferentation). We use a recurrent neural network model [2] as a vehicle to study structural plasticity; to study the time course of synaptic rewiring following a lesion, we represent the synapse as consisting of axonal (terminals/varicosities) and dendritic elements (spines). Independent development of both pre- and postsynaptic elements allows for modelling synapse formation, pruning and synaptic turnover as distinct processes. Model neurons increase and decrease axonal and dendritic elements in an activity-dependent fashion. Hence, synaptic rewiring is subject to shifts in the excitation-inhibition equilibrium. We apply this model to recent experimental data from Keck et al. [3] on cortical remapping following focal retinal lesion. The model could also be applied to somatosensory deafferentation. In this study we demonstrate that maintaining network homeostatis and rebalancing deafferented neurons by synaptic rewiring can result in post-lesion cortical remapping. Thus, the model bridges the gap between activity-dependent morphological changes on the neuronal level and a changing connectivity of cortical maps on an anatomical level. These theoretical results could have large consequences for neurological rehabilitation after stroke.

References

  1. Butz M, Wörgötter F, van Ooyen A: Activity-dependent structural plasticity.

    Brain Res Rev 2009, in press. PubMed Abstract | Publisher Full Text OpenURL

  2. Butz M, Teuchert-Noodt G, Grafen K, van Ooyen A: Inverse relationship between adult hippocampal cell proliferation and synaptic rewiring in the dentate gyrus.

    Hippocampus 2008, 18:879-898. PubMed Abstract | Publisher Full Text OpenURL

  3. Keck T, Mrsic-Flogel TD, Vaz Afonso M, Eysel UT, Bonhoeffer T, Hübener M: Massive restructuring of neuronal circuits during functional reorganization of adult visual cortex.

    Nat Neurosci 2008, 11:1162-1167. PubMed Abstract | Publisher Full Text OpenURL