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Epileptogenesis is a complex and not well understood phenomenon. It has been largely described as pathology occurring because of an imbalance between excitatory and inhibitory brain networks. Through our experiments we attempted to show that epileptogenesis could be “hijacking” the brain mechanisms responsible for memory formation. We began by using an associative experimental design, pairing auditory and visual cues with electrically kindled evoked seizures to design a rodent model of reflex seizures. Reflex seizures are a clinical phenomenon characterized by convulsive episodes induced by specific sensory stimuli or cognitive actions. Our experiment failed to establish a reflex seizure model in rodents, but interestingly we observed behavior and electrophysiology similar to fear conditioning, with significant freezing in animals paired with cues. Using the same animals, we investigated memory reconsolidation blocking therapies, which rely upon replaying neuronal activity but instead of strengthening, involved synapses are weakened. We used rapamycin to weaken neuronal circuitry replayed with the sensory cues and evoked seizures to weaken epileptic networks. Although this was aimed as an exploratory study, the drug therapy abolished seizures in two animals, demonstrating promising results.

Epileptogenesis is a complex and not well understood phenomenon. It has been largely described as pathology occurring because of an imbalance between excitatory and inhibitory brain networks. Through our experiments we attempted to show that epileptogenesis could be “hijacking” the brain mechanisms responsible for memory formation. We began by using an associative experimental design, pairing auditory and visual cues with electrically kindled evoked seizures to design a rodent model of reflex seizures. Reflex seizures are a clinical phenomenon characterized by convulsive episodes induced by specific sensory stimuli or cognitive actions. Our experiment failed to establish a reflex seizure model in rodents, but interestingly we observed behavior and electrophysiology similar to fear conditioning, with significant freezing in animals paired with cues. Using the same animals, we investigated memory reconsolidation blocking therapies, which rely upon replaying neuronal activity but instead of strengthening, involved synapses are weakened. We used rapamycin to weaken neuronal circuitry replayed with the sensory cues and evoked seizures to weaken epileptic networks. Although this was aimed as an exploratory study, the drug therapy abolished seizures in two animals, demonstrating promising results.

Epileptogenesis is a complex and not well understood phenomenon. It has been largely described as pathology occurring because of an imbalance between excitatory and inhibitory brain networks. Through our experiments we attempted to show that epileptogenesis could be “hijacking” the brain mechanisms responsible for memory formation. We began by using an associative experimental design, pairing auditory and visual cues with electrically kindled evoked seizures to design a rodent model of reflex seizures. Reflex seizures are a clinical phenomenon characterized by convulsive episodes induced by specific sensory stimuli or cognitive actions. Our experiment failed to establish a reflex seizure model in rodents, but interestingly we observed behavior and electrophysiology similar to fear conditioning, with significant freezing in animals paired with cues. Using the same animals, we investigated memory reconsolidation blocking therapies, which rely upon replaying neuronal activity but instead of strengthening, involved synapses are weakened. We used rapamycin to weaken neuronal circuitry replayed with the sensory cues and evoked seizures to weaken epileptic networks. Although this was aimed as an exploratory study, the drug therapy abolished seizures in two animals, demonstrating promising results.