Different mechanisms of hypersynchrony initiation lead to divergent transcriptome changes in the mouse forebrain

Sodium and potassium channelopathies could lead to seizures and epilepsy through two broad mechanisms: aberrant activity of excitatory neurons, or decrease of GABAergic neuron excitability leading to disinhibition. It is currently unknown whether these two modes of seizure induction lead to similar changes in the brain transcriptome. To address this questions, we performed RNAseq on the cortex and hippocampus of P15 Kcnq2Flx/Flx::Emx1-Cre+ and Scn1aA1783V/+::Slc32a1-Cre+ mice that both have seizures and do no survive past weaning age. Overall design: RNAseq of cortices and hippocampi of 3 Kcnq2 Flx/Flx::Emx1-Cre+ and 3 littermate control mice. RNAseq of hippocampi of 3 Scn1aA1783V/+::Slc32a1-Cre+ and 3 littermate control mice.