The major focus of my laboratory is on developing new age-specific therapies for epilepsy and its comorbidities. We specifically focus on forms of epilepsy that affect the infant and early childhood brain, and have extensive expertise in investigations of human tissue as well as rat and mouse models of early life epilepsy. Our interests have been on hypoxic/ischemic injury and seizures in the perinatal and young postnatal brain. My lab has published expertise in cellular and regional alterations in synaptic proteins and signaling pathways using whole animal, human tissue, and in vitro brain slices and cell cultures. Almost 20 years ago we showed that hypoxia can induce seizures in the neonatal brain and this increased network excitability in adulthood; over the years we have worked to show that AMPARs are involved in this epileptogenesis and that spontaneous seizures are increased in adulthood, confirming this as a model of epileptogenesis.
We also discovered if seizures occur during the critical period of early brain development, synaptic plasticity mechanisms are dysregulated to produce epilepsy–induced synaptic potentiation, and importantly in addition to impairing Hebbian plasticity, there is also an autistic–like behavioral phenotype. Hence our interest in understanding the interaction in epilepsy and autism/neurodevelopmental delay. Along these lines, we discovered alterations of the mTOR pathway following early life seizures and injury in the wild type rat brain, and a protective role for rapamycin in preventing long term epilepsy and autistic–like behavior.