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Predictions in Absence Epilepsy with the use of Computer Models of Neuronal Networks

p. 209-222

Abstract

A computer model of a thalamic network was used in order to understand the rhythmic activity that characterizes absence epilepsy. The model was constructed using a Hodgkin Huxley framework. Results from the model confirm the hypothesis that an isolated augmentation of the maximum conductance of the low threshold calcium current (IT) in the reticular thalamic nucleus may be conducive to the occurrence of autorhythmicity and hence epilepsy. The model predicts that higher values of this IT can cause the transition of the network to an intermittent state. This intermittency increased monotonically with the increase of IT in the reticular nucleus. The model was also used to investigate electrophysiological methods of bringing about a transition of the network to a subthreshold state. Methods that were successful at bringing about a phase shift that resulted in the reticular thalamic neurons firing before the thalamocortical neurons were found to lead to subthreshold activity in the network. This sort of phase shift was attained either by the application of periodic excitatory pulses to the reticular thalamic neurons or the application of a constant hyperpolarization to the thalamocortical neuron.

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References

Bibliographical reference

Elizabeth Thomas and Thierry Grisar, « Predictions in Absence Epilepsy with the use of Computer Models of Neuronal Networks », CASYS, 1 | 1998, 209-222.

Electronic reference

Elizabeth Thomas and Thierry Grisar, « Predictions in Absence Epilepsy with the use of Computer Models of Neuronal Networks », CASYS [Online], 1 | 1998, Online since 05 July 2024, connection on 26 December 2024. URL : http://popups.uliege.be/3041-539x/index.php?id=1125

Authors

Elizabeth Thomas

Institut Léon Fredericq – Université de Liège, 17 Place Delcour – 4000 Liège, Belgium

Thierry Grisar

Institut Léon Fredericq – Université de Liège, 17 Place Delcour – 4000 Liège, Belgium

Copyright

CC BY-SA 4.0 Deed