Network models of absence seizures.

Alain Destexhe

In: Neuronal Networks in Brain Function, CNS Disorders and Therapeutics, Edited by Faingold, C.L. and Blumenfeld, H., Elsevier, Amsterdam, pp. 11-35, 2014.

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Abstract

Absence seizures result from complex interactions involving the thalamus and cerebral cortex, and were investigated in humans as well as in several animal models. The genesis of absence seizures depends on different neuron types, their nonlinear properties such as burst generation, and the different receptor types present in thalamocortical circuits. These details can be incorporated into computational models to investigate such interactions, and point to possible mechanisms by which seizures can be generated and sustained by those circuits. The present chapter overviews the search for mechanisms of absence seizures, by successively reviewing the contribution of thalamic circuits, cortical circuits and finally the thalamocortical system. Models suggest that a key to explain absence seizures is the massive cortico-thalamic feedback and its capability to switch the entire system to hypersynchronized discharges at 3 Hz, due to the nonlinear properties of GABA-B receptors. This mechanism accounts for observations in human absence epilepsy and is consistent with several experimental models of absence seizures in cats, rats and mice. It provides an explanation for the different frequencies of seizures in rodents (5-10 Hz) compared to 3 Hz seizures in higher mammals. Such models should be useful as a guide to identify possible targets to suppress seizures, such as specific synaptic receptor types or ion channels.
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