Glucocorticoid resistance during chronic social stress in mice: RNA-seq of prefrontal cortex

Chronic stress often leads to the development of various psychopathologies and is usually associated with a change in the function of the HPA axis. An elevated level of glucocorticoid (GC) hormones in the blood initially causes an acute reaction of the body, which subsequently fades, even with continued stimulation with glucocorticoids. It is known that the degree of resistance to elevated hormone levels can affect the effectiveness of therapy in the treatment of stress-induced psychopathologies. In order to identify the molecular basis for the formation of GC resistance, we analyzed the effect of chronic social stress on the transcriptome of the prefrontal cortex in an experimental model of depression. We assessed the level of gene expression in the prefrontal cortex of the control C57BL/6 mice and mice with stress experience for 30 days, both in the basal state and with additional stimulation with dexamethasone. The introduction of dexamethasone made it possible to simulate the situation of an increase in the level of glucocorticoids and activation of the glucocorticoid receptor.