GSK3B and epilepsy: Despite the increased GSK3β activity having been probed in other epilepsy models (Lohi et al., 2005; Tripathi et al., 2010; Lee et al., 2012), the addition of KA into hippocampal slices of mice that overexpressed a constitutively active form of GSK3β produced a decreased progression of induced epileptogenesis, probably mediated by the reduced phosphorylation of the GluA1 subunit of the glutamate α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor (Urbanska et al., 2019).