Our lab seeks to understand the secret life of the fetal and infant brain. In particular, we are studying the development of activity in the cerebral cortex and its connected subcortical structures. Our goal is to identify the early circuit changes that cause the maturation of brain activity. Using an animal model and EEG data from human infants born pre-term, we study how network changes are related to changes in infant behavior, and how they support brain and cognitive maturation. ​Far from being a passive recipient of information from the outside world, our work is beginning to reveal active mechanisms used by the fetal brain to shape activity into a form uniquely suited for its own development. Our work on a validated animal model of fetal development has documented several unique specializations of the fetal and infant brain. These include: ​1) "Booster" circuits that amplify weakly connected inputs such as those from the infant's retina to the thalamus. 2) An all-or-none "Bursting" mode of information processing by fetal cortex, that switches to the mature, higher resolution "Acuity" mode just before birth. This means the fetal brain is unlikely to process complex stimuli (like Mozart), in a normal way. 3) A complete absence of the ability to generate a state of wakefulness in cortex until just before the onset of high-quality sensory experience at eye opening (or birth in humans). Having a normal timeline of fetal cortical activity development in rats, mice, and humans is an important first step to identifying disrupted circuits in animal models of disease. We are using this normal timeline to identify deviations in the development of cortical activity in animal models of neurodevelopmental disorders. ​Using this approach, we have identified several new phenotypes in the rat model of Fragile X syndrome, at ages earlier than symptoms are usually observed. For example, we have found a paradoxical arousal in the cortex of infant Fragile X rats when the animal is behaviorally at rest. This suggests that unlike their wild-type littermates, infant Fragile X rats are unable to suppress cortical arousal to unattended stimuli. This approach has also allowed us to identify which activity appears to develop normally. For example, the developmental trajectory of spontaneous activity is relatively normal in infant Fragile X rat cortex, but visual evoked activity is hypo-excitable.