Neurological disorders can be caused by genetic alterations in many genes; UBE3A is one such gene, as a mutation or deletion in the maternal copy of this gene has been shown to cause Angelman Syndrome (AS). AS is a developmental disorder that affects 1 in 15,000 live births, and is characterized by many symptoms, with seizures being highly penetrant and debilitating. Previous research on the pathological characterization of AS model mice showed an increased seizure susceptibility as well as abnormally high levels of perineuronal net (PNN) fluorescence. Our project aims to determine whether the increased PNNs in the dentate gyrus of the hippocampus may be responsible for this enhanced seizure susceptibility. Mice were exposed to flurothyl in order to determine differences in seizure susceptibility and better understand the emergence of the enhanced PNN deposition seen in AS model mice. We found that AS mice become more susceptible to seizures throughout the incubation period, with a simultaneous increase in PNN fluorescence. Also, degrading PNNs appear to have a slight protective effect in AS model mice. These results may indicate a possible therapeutic target for AS individuals suffering from otherwise intractable seizures.