Inhibition sculpts neuronal structure and function during adolescence: implications for mood and learning α4βδ GABAA receptors increase expression at puberty in the mouse hippocampus where they generate a tonic inhibition. Because these receptors express on the dendritic spine adjacent to excitatory synapses, my lab is interested in the role this developmentally-regulated inhibition plays in cognition and synaptic pruning of dendritic spines during adolescence, which impacts behavioral flexibility in adulthood. This receptor is also the target for neurosteroids which alter mood. Adolescence is a vulnerable period for the development and exacerbation of disorders such as anxiety as well as autism and schizophrenia, which are also interests of the lab. Neuronal circuits in the hippocampus underlie spatial learning and, as part of the limbic system, also play a role in the development of anxiety. My laboratory studies how the activity of these circuits is sculpted by inhibition generated by GABAA receptors, which can then lead to changes in cognition, mood and pathological states such as epilepsy. Our most recent studies focus on changes generated by inhibition during the period of adolescence, a critical period for certain types of learning and when certain neuropsychiatric disorders, such as anxiety and schizophrenia first develop. Our primary focus is the α4βδ GABAA receptor, a membrane protein which emerges at the onset of puberty on the dendrites and spines of pyramidal cells in the CA1 hippocampus and other CNS areas.