The Genetic Absence Epilepsy Rat from Strasbourg (GAERS) is a well-validated rodent model of absence epilepsy4.
Klein JP, Khera DS, Nersesyan H, Kimchi EY, Waxman SG, Blumenfeld H. Dysregulation of sodium channel expression in cortical neurons in a rodent model of absence epilepsy.
Tsakiridou, E., Bertollini, L., de Curtis, M., Avanzini, G. & Pape, H. C. Selective increase in T-type calcium conductance of reticular thalamic neurons in a rat model of absence epilepsy.
Powell, K. L. et al. A Cav3.2 T-type calcium channel point mutation has splice-variant-specific effects on function and segregates with seizure expression in a polygenic rat model of absence epilepsy.
Talley, E. M., Solorzano, G., Depaulis, A., Perez-Reyes, E. & Bayliss, D. A. Low-voltage-activated calcium channel subunit expression in a genetic model of absence epilepsy in the rat.
For this, activation of either the rostral or caudal parts of the deep and intermediate layers of the superior colliculus was applied in a genetic model of absence seizures in the rat (GAERS).
Here we describe the use of brain punch micro-sampling, used in combination with commercially available cDNA arrays, for profiling brain gene expression in a mutant strain of rat (GAERS model of absence epilepsy).
In vivo, 45 suppressed seizure frequency in a rat model of absence epilepsy and showed significant alterations of sleep architecture after oral dosing to rats as measured by EEG.
Lethargic (lh/lh) mice, which function as an animal model of absence seizures, have spontaneous seizures that have behavioral and electrographic features and anticonvulsant sensitivity similar to those of human absence seizures.
This behaviour has also been observed in a more detailed, higher dimensional model of interacting neural masses used as a model of absence epilepsy, so our results suggest that there is an underlying bifurcation mechanism leading to this type of dynamics.
