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This article is part of the supplement: Eighteenth Annual Computational Neuroscience Meeting: CNS*2009

Open Access Poster presentation

GABAA receptor plasticity provides homeostasis of neuronal activity in a neocortical microcircuit model

Ronald AJ van Elburb12*, Laurens WJ Bosman3, Margreet C Ridder1, Arjen B Brussaard1 and Arjen van Ooyen1

Author Affiliations

1 Department of Integrative Neurophysiology, Center for Neurogenomics and Cognitive Research, VU University Amsterdam, The Netherlands

2 Department of Artificial Intelligence, Faculty of Mathematics and Natural Sciences, University of Groningen, The Netherlands

3 Department of Neuroscience, Erasmus Medical Center, Rotterdam, The Netherlands

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BMC Neuroscience 2009, 10(Suppl 1):P218  doi:10.1186/1471-2202-10-S1-P218


The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1471-2202/10/S1/P218


Published:13 July 2009

© 2009 van Elburb et al; licensee BioMed Central Ltd.

Poster presentation

During the eye-opening development phase in mice, in primary visual cortex, changes in GABAA postsynaptic receptor function appear to occur in a highly regulated manner. In particular, significant correlation [1,2] exists between the developmental reduction in the duration of inhibitory postsynaptic currents (IPSCs) and the concomitant developmental changes in total inhibitory synaptic weight (Figure 1). Using a computational model [3], we characterize the extent to which GABAA receptor plasticity and changes in synaptic weight affect the input-output transfer of a neocortical microcircuit consisting of pyramidal cells with reciprocal synaptic connections to perisomatic innervating interneurons. We found that when developmental GABAA receptor plasticity is matched by a gradual shift in overall inhibitory synaptic weight, input-output constancy is created with respect to both firing frequency (Figure 2) and spike train patterning. We propose that GABAA receptor plasticity matches the concomitant shift in synaptic weight per neuron in order to guarantee homeostasis of microcircuit function. We discuss the putative relevance of such a regulatory mechanism in terms of neocortical development. In addition to demonstrating homeostasis of neuronal activity during maturation of the GABAergic synaptic network, we show that IPSC decay affect burst firing, that accelerating the IPSC decay appears to reduce the extent of flicker fusion, and that changing the IPSC decay provides the microcircuit with a synaptic mechanism for gain modulation.

thumbnailFigure 1. Changes in GABAergic neurotransmission during neonatal development. Relationship between sIPSC frequencies and decay time constants during postnatal development of the rat visual cortex. Shown are the average values for each neuron measured.

thumbnailFigure 2. Homeostasis of firing frequency during neonatal development. For different input frequencies, the output frequency of the microcircuit is shown as a function of both inhibitory synaptic weight and IPSC decay time.

References

  1. Bosman LW, Rosahl TW, Brussaard AB: Neonatal development of the rat visual cortex: synaptic function of GABAA receptor alpha subunits.

    J Physiology 2002, 545:169-181. Publisher Full Text OpenURL

  2. Heinen K, Bosman LW, Spijker S, van Pelt J, Smit AB, Voorn P, Baker RE, Brussaard AB: GABAA receptor maturation in relation to eye opening in the rat visual cortex.

    Neuroscience 2004, 124:161-171. PubMed Abstract | Publisher Full Text OpenURL

  3. van Elburg RAJ, van Ooyen A: Generalization of the event-based Carnevale-Hines integration scheme for integrate-and-fire models.

    Neural Computation 2009, in press. PubMed Abstract | Publisher Full Text OpenURL