Corticosterone, the principal glucocorticoid in rodents, through GRs, increases dopaminergic activity in mesocorticolimbic areas, and reduced GR sensitivity is suggested to increase vulnerability to addiction [18]. Chronic corticosterone administration, which mimics chronic stress, leads to reorganization of the cortical neuronal circuits, likely compromising their top-down inhibitory function exerted on amygdala (Amy) activity [19, 20]. Under stressful conditions, greater Amy activity leads to increased dopamine levels in the nucleus accumbens (Acb) and medial prefrontal cortex (mPFC) possibly through stimulation of the ventral tegmental area (VTA) [18, 19].
