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. Author manuscript; available in PMC: 2019 Jan 1.
Published in final edited form as: Epilepsia. 2017 Dec 18;59(1):135–145. doi: 10.1111/epi.13962

Table 1.

Wild type and P640L Channel Electrophysiology and Predicted Network Effects

Glauser et al Electrophysiology Results
Ethosuximide 0 mM 3 mM
Channel Type Wild P640L Variant Wild P640L Variant
Conductance 100% 100% 98% 102%
Shift of SS Activation / Inactivation Window (mV) 0 2 −7.5 −11
Inactivation Time Constant Tau (ms) 19.8 18.1 14.2 (5.7ms decrease) 16.2 (1.9ms decrease)
Model Predicted Network Effects
Ethosuximide 0 mM 3 mM
Channel Type Wild P640L Variant Wild P640L Variant
 Conductance No effect No effect
 Shift SS Activation / Inactivation Window No effect No effect
 Inactivation Time Constant Tau No effect Large decrease in SW (Fig 5A) Small decrease in SW (Fig 5B)

The upper portion of the table summarizes changes in wild type and P640L variant T-Type Calcium Channel Electrophysiology when exposed to ethosuximide as reported by Glauser et al. The lower portion of the table shows the network effect the model predicts for each change in T-type calcium channel parameters. Statistically significant differences in T-type calcium channel parameters from baseline that emerged during electrophysiology experiments are highlighted in bold. Note that although ethosuximide caused a significant right shift in steady state activation/inactivation, the model predicts that this change will not alter overall network behavior. In contrast, the model predicts that decreased inactivation time constant will treat seizure (convert spike and wave oscillations to spindle oscillations) for an area in parameter space. This effect is reduced for the variant calcium channel (see Fig 5).