Loss of presenilin 2 function increases susceptibility to kainate‐induced status epilepticus and attenuates associated increases in hippocampal kainate‐type glutamate receptor expression

Loss of normal PSEN2 function increases susceptibility to KA-induced seizures and SE, which cannot be explained by basal GluK5 expression differences. However, increased GluK5 expression in male WT relative to PSEN2-KO mice 7-days post KA-SE, further substantiates a role of PSEN2 in KAR availability. Sex differences in GluK5 and GFAP were also apparent post-SE.