My lab is primarily focused on understanding neurobiological mechanisms that control vulnerability to traumatic stress. In particular, we are interested in tracing how early-life exposure to obesogenic environments results in (mal)adaptive neuroplasticity. A common thread among our studies is the use of clinically relevant diet-induced obesity and post-traumatic stress disorder (PTSD) models to define the relative contribution and mechanisms by which obesogenic diets and toxic stress modulate corticolimbic circuit maturation, neuronal plasticity, and susceptibility during adolescence.