Fig. 7.

Molecular pathogenic model of gene repression in epileptogenesis. The present in-vitro model some captures electrophysiological and molecular features of epileptogenesis on a compressed scale. The latent period after glutamate (Glu) injury was characterized by silencing of epilepsy candidate genes (black line) through convergent action of different epigenetic mechanisms including locus-specific loss of histone acetylation (green), transient increase in H3K9 (red) and H3K27 trimethylation (light blue), and accumulation of DNA methylation at respective gene promoters (dark blue; dotted and solid lines indicate different possible pathogenic time courses for DNA methylation accumulation), associated gradual onset of neuronal spiking activity after 3 days and later synchronization of neuronal hyperactivity as well as a change in signal towards bursting activity after 7 days