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This article is part of the supplement: Sixteenth Annual Computational Neuroscience Meeting: CNS*2007

Open Access Poster presentation

The role of glia in seizures

Ghanim Ullah1*, John R Cressman1, Ernest Barreto2 and Steven J Schiff13

Author Affiliations

1 Center for Neural Engineering, Department of Engineering Science and Mechanics, Pennsylvania State University, University Park, PA 16802, USA

2 Krasnow Institute for Advanced Study, George Mason University, Fairfax, VA 22030, USA

3 Department of Neurosurgery, Pennsylvania State University, University Park, PA 16802, USA

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BMC Neuroscience 2007, 8(Suppl 2):P28  doi:10.1186/1471-2202-8-S2-P28

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

Published:6 July 2007

© 2007 Ullah et al; licensee BioMed Central Ltd.


We present an ionic current model, composed of Hodgkin-Huxley type neurons and glia designed to investigate the role of potassium in the generation and evolution of neuronal network instabilities leading to seizures. We show that such networks reproduce seizure-like activity if glial cells fail to maintain the proper extracellular K+ concentration.


Our neuronal network model combines the Hodgkin-Huxley type of formulism for the neuronal currents with a model for the dynamics of extra and intracellular K+ concentration controlled by a glial network. The equations for the ionic currents are adopted from the model in ref. [1]. The extra and intracellular K+ concentrations are calculated based on various K+ currents.


We investigate the instability in cortical networks by studying two interacting one-dimensional networks consisting of 100 pyramidal cells and 100 interneurons. The network exhibits persistent and spatially confined activity in a parameter range where inhibition is balanced by excitation. We then find various physiologic conditions under which a network displaying a stable persistent activity can switch to seizure like states.


The main finding of our study is that the network activity packet is stable provided that (1) the excitable synaptic strength is not very high; (2) the extracellular potassium concentration is low enough to be well in the physiological range (i.e. the glial network is functioning efficiently); and (3) perturbations to the network are not very strong.


Supported by NIH grants ROIMH50006 and K02MH01493.


  1. Gutkin BS, Laing CR, Colby CL, Chow CC, Ermentrout GB: Turning on and off with excitation: the role of spike-timing asynchrony and synchrony in sustained neural activity.

    J Comput Neurosci 2001, 11:121-134. PubMed Abstract | Publisher Full Text OpenURL