[Abstract Title]. - Society for Neuroscience

Poster
250. Epilepsy: Networks
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 250.14/V26
Topic: B.09.d. Oscillations and synchrony: Other
Support: Australian Research Council
Title: Modeling absence seizure dynamics: implications for network and cellular mechanisms
Authors: *J. A. ROBERTS 1,3 , P. A. ROBINSON 1,2,3 ;
1 Sch. Physics, 2 Fac. Med., Univ. Sydney, Sydney, Australia; 3 Brain Dynamics Center, Westmead
Millenium Inst., Westmead Hosp. and Univ. Sydney, Westmead, Australia
Abstract: The relative contributions of network and cellular mechanisms to absence seizures are
not yet fully understood. Oscillations in corticothalamic loops have been observed, with debate
over the roles of local mechanisms in the cortex and thalamus. We use a physiologically-based
mean-field model of the interconnected cortex and thalamus to determine the relative
contributions of axonal and intrinsic cellular delays to the waveforms of absence seizures. Our
model has previously been shown to successfully reproduce both the healthy human
electroencephalogram and 3 Hz oscillations corresponding to absence seizures under plausible
parameter changes in the corticothalamic loop. The predicted period of the absence seizure
depends linearly on model parameters describing thalamocortical, corticothalamic, intracortical,
synaptic, and dendritic delays, and these dependences are linked to the seizure mechanism by
showing how time intervals between peaks in the waveforms depend on the parameters. We
show that a corticothalamic loop mechanism for absence seizures is consistent with intrathalamic
cellular properties being the leading determinant of the frequency of spike-wave discharges in rat
genetic models, while properties of the corticothalamic loop play a greater role in humans.
Furthermore, the lower frequency of human absence seizures compared to spike-wave discharges
in the rat can be attributed to longer propagation delays in the corticothalamic loop, without
needing different cellular properties.
Disclosures: J.A. Roberts, None; P.A. Robinson, None.
Poster