Epilepsy is the 3rd most common neurological disease, and it affects both humans and animals. Epileptogenesis is how an individual develops epilepsy and is typically caused by neuronal hyperexcitability. Antiepileptic drugs target ion channels to reduce neuronal hyperexcitability, but more than one-third of epileptic patients do not respond to treatments. There are around 30 antiepileptic drugs and about 45 other drugs that have failed clinical trials. The goal of this study was to find alternative pathways to aid in drug development. Neuroinflammation was the alternative target pathway studied. A rat model was used, and epileptogenesis was induced with the chemical nerve agent diisopropylfluorophosphate. Once epilepsy was established, one group was treated with the drug saracatinib and the other a control. The rats were then surrendered under terminal anesthesia, and brains were collected for dissection. Once dissected, portions of the brain underwent immunohistochemistry stains so that imaging with a fluorescent microscope could be done. Images helped to find the portions of the brain where neuroinflammation occurred. Data showed that the use of saracatinib resulted in the lowest total astrocyte counts. Currently, saracatinib is a leading drug used in Alzheimer's research. Saracatinib works to both inhibit inflammatory pathways as well as excitotoxicity in neurons. We hoped that administration early into epileptogenesis would lead to a reduction in epileptic markers.