Extending Human Genome-Wide “Omics” Data With Mechanistic Studies in Rodent Models Identifies an Astrocyte-specific Mechanism of Orbitofrontal Cortex Dysfunction in Major Depressive Disorder

Overall risk for Major Depressive Disorder (MDD) is determined by complex interactions between genetic and environmental factors that influence epigenetic regulation of neuroplasticity and stress pathways. These mechanisms are specific to the distinct regulatory context within regionally-defined brain cell-types. Here, we employed genome-wide chromatin accessibility profiling of neuronal vs. non-neuronal cells in orbitofrontal cortex (OFC) to capture regulatory signatures of MDD.