Animal models of epilepsy are critical in drug development and therapeutic testing. However, dominant methods for evaluating epilepsy treatments face a tradeoff between higher throughput and etiological relevance. Screening models are either based on acutely induced seizures in wild-type, naive animals or spontaneous seizures in chronically epileptic animals. Each has its disadvantages – acute convulsant or kindling-induced seizures do not account for the myriad neuropathological changes in the diseased, epileptic brains, and spontaneous behavioral seizures are sparse in chronically epileptic models, making it time-intensive to sufficiently power experiments. In this study, we developed the Opto-IHK (optogenetically induced seizures in intrahippocampal kainate mice) model, a mechanistic approach to precipitate seizures ‘on demand’ in chronically epileptic mice. We briefly synchronized principal cells in the CA1 region of the diseased hippocampus to reliably induce stereotyped on-demand