Cognitive and social deficits are core to most psychiatric diseases. Dysfunctional connectivity in brain networks, including the prefrontal cortex (PFC) and its interacting subcortical structures, is supposed to elicit these deficits. Stress exposure and the ensuing release of glucocorticoid hormones is a common risk factor for psychiatric diseases and is known to modulate cognitive function partly through its binding to its receptor GR. The general aim of this work is to study the impact of stress exposure on PFC function and its extended brain networks. As expected, we show here that repeated social defeat leads to an impairment in social abilities. We further show that cognitive flexibility in a set-shifting task is also impacted. Pharmacogenetic inhibition of the inputs from the dorsal thalamus to the PFC leads to a decrease in social interaction. Experiments on cognitive flexibility are ongoing. Repeated social defeat also leads to a decrease in GR expression within the PFC. Inactivating neuronal GR in this brain region recapitulates the impact of stress exposure on cognitive flexibility. Altogether, these data point toward the PFC and potentially thalamo-prefrontal networks as key for stress-induced cognitive and social deficits. Further experiments will be needed to investigate the physiological impact of stress exposure in these circuits.