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Background

Neural circuit disruptions have been increasingly appreciated as contributing directly to psychiatric dysfunction, making the identification of such disruptions extremely promising as therapeutic targets. Identifying molecular contributors to specific neural circuit activity may provide a more promising route to efficacious drugs that target specific circuit-level causes of psychiatric dysfunction. In order to dissect the ways in which gene, cells, and neural circuits coordinate to depressive-like response to chronic stress, we employed a multidisciplinary approach using in vivo neurophysiology and RNA-Seq in a mouse model of chronic social stress.

Methods

Using in vivo neurophysiology in freely behaving mice, we recorded an endophenotype of stress-susceptibility: pre-frontal cortex 2-7Hz oscillatory activity. We then measured the reactivity of this neural signature in a preclinical model of the ‘aggressive faces …