Skip to content


You're viewing the new version of our site. Please leave us feedback.

Learn more

BMC Neuroscience

Open Access

The role of glia in seizures

  • Ghanim Ullah1Email author,
  • John R CressmanJr1,
  • Ernest Barreto2 and
  • Steven J Schiff1, 3
BMC Neuroscience20078(Suppl 2):P28

Published: 6 July 2007


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.

Authors’ Affiliations

Center for Neural Engineering, Department of Engineering Science and Mechanics, Pennsylvania State University
Krasnow Institute for Advanced Study, George Mason University
Department of Neurosurgery, Pennsylvania State University


  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. 10.1023/A:1012837415096.PubMedView ArticleGoogle Scholar


© Ullah et al; licensee BioMed Central Ltd. 2007

This article is published under license to BioMed Central Ltd.