My lab aims to investigate the developmental mechanisms of cortical circuit assembly and function. We are interested in two main questions: First, how does sensory experience and learning shape the connectivity and function of inhibitory neurons during cortical sensory processing; and secondly how do genetic and environmental factors alter inhibitory interneuron function leading to sensory processing deficits in neurodevelopmental and neuropsychiatric disorders. We are particularly interested in how inhibitory interneurons in the auditory and visual cortices integrate bottom-up sensory inputs together with top-down feedback to mediate these processes. Higher order projections to sensory cortical areas converge on layer 1 (L1), the primary site for integration of top-down information via the apical dendrites of pyramidal neurons and L1 GABAergic interneurons. I will discuss our recent study that investigated the contribution of early thalamic inputs onto L1 interneurons for the establishment of top-down connectivity in the primary visual cortex. We found that bottom-up thalamic inputs predominate during L1 development and preferentially target neurogliaform cells. 

Interestingly,  these projections were found to be critical for the subsequent strengthening of top-down inputs from the anterior cingulate cortex onto L1 neurogliaform cells. Sensory deprivation or selective removal of thalamic afferents blocked this phenomenon. While early activation of the anterior cingulate cortex resulted in a premature strengthening of these  top-down afferents, this was dependent on thalamic inputs. We are currently investigating how the balance between bottom-up and top-down signaling onto L1 interneurons is disrupted in neuropsychiatric disorders such as autism and schizophrenia.