PERK is known to play key regulatory roles on endoplasmic reticulum homeostasis and it is essential for the normal function of secretary cells in the pancreas and skeletal system. A tissue specific, PERK knock out mouse model has an ablation of PERK specific to the brain (BrPERK-KO). These mice were initially observed having random seizures, those not previously observed in mice in our laboratory. Seizure susceptibility tests were conducted between Wild type, BrPERK-KO, and Lox-P strain mice and the results were analyzed. WT and Lox-P strain mouse models showed similar levels of PERK expression that were greater than the BrPERK-KO strain. The mice without PERK in the forebrain show a trend towards a shorter latency to seizure development than their counterparts with normal PERK expression in the forebrain. Due to the similarity of pancreatic beta cells and neuronal cells and PERK’s known role in regulating calcium dynamics in the pancreas, we hypothesize that PERK may play a role in neuronal calcium dynamics as well.