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Knox implementation of Destexhe 1998 spike and wave oscillation model (Knox et al 2018)
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" ...The aim of this study was to use an established thalamocortical computer model to determine how T-type calcium channels work in concert with cortical excitability to contribute to pathogenesis and treatment response in CAE. METHODS: The model is comprised of cortical pyramidal, cortical inhibitory, thalamocortical relay, and thalamic reticular single-compartment neurons, implemented with Hodgkin-Huxley model ion channels and connected by AMPA, GABAA , and GABAB synapses. Network behavior was simulated for different combinations of T-type calcium channel conductance, inactivation time, steady state activation/inactivation shift, and cortical GABAA conductance. RESULTS: Decreasing cortical GABAA conductance and increasing T-type calcium channel conductance converted spindle to spike and wave oscillations; smaller changes were required if both were changed in concert. In contrast, left shift of steady state voltage activation/inactivation did not lead to spike and wave oscillations, whereas right shift reduced network propensity for oscillations of any type...."
Knox AT, Glauser T, Tenney J, Lytton WW, Holland K (2018) Modeling pathogenesis and treatment response in childhood absence epilepsy.
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Thalamus reticular nucleus GABA cell;
Thalamus geniculate nucleus/lateral principal GLU cell;
Neocortex layer 4 pyramidal cell;
Neocortex fast spiking (FS) interneuron;
I T low threshold;
Knox, Andrew [knox at neurology.wisc.edu];
Destexhe, Alain [Destexhe at iaf.cnrs-gif.fr];
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Thalamus geniculate nucleus/lateral principal GLU cell
Thalamus reticular nucleus GABA cell
I T low threshold
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