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J Comput Neurosci. 2019 Apr;46(2):197-209. doi: 10.1007/s10827-019-00711-x. Epub 2019 Feb 9.

Outgrowing seizures in Childhood Absence Epilepsy: time delays and bistability.

Author information

1
Department of Applied Mathematics, University of Waterloo, Waterloo, ON, N2L 3G1, Canada.
2
Institute of Applied Mathematics and Department of Mathematics, University of British Columbia, Vancouver, BC, V6T 1Z2, Canada.
3
W.M. Keck Science Department, The Claremont Colleges, Claremont, CA, 91711, USA.
4
Department of Applied Mathematics and Centre for Theoretical Neuroscience, University of Waterloo, Waterloo, ON, N2L 3G1, Canada. sacampbell@uwaterloo.ca.

Abstract

We formulate a conductance-based model for a 3-neuron motif associated with Childhood Absence Epilepsy (CAE). The motif consists of neurons from the thalamic relay (TC) and reticular nuclei (RT) and the cortex (CT). We focus on a genetic defect common to the mouse homolog of CAE which is associated with loss of GABAA receptors on the TC neuron, and the fact that myelination of axons as children age can increase the conduction velocity between neurons. We show the combination of low GABAA mediated inhibition of TC neurons and the long corticothalamic loop delay gives rise to a variety of complex dynamics in the motif, including bistability. This bistability disappears as the corticothalamic conduction delay shortens even though GABAA activity remains impaired. Thus the combination of deficient GABAA activity and changing axonal myelination in the corticothalamic loop may be sufficient to account for the clinical course of CAE.

KEYWORDS:

Childhood absence epilepsy; Time delay

PMID:
30737596
DOI:
10.1007/s10827-019-00711-x

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