Glucocorticoid neurodynamics are the most crucial determinant of the hormonal effects in the mammalian brain, and depend on multiple parallel receptor and enzymatic systems, responsible for effectively binding with the hormone (and mediating its downstream molecular effects) and altering the local glucocorticoid content (by adding, removing or degrading glucocorticoids), respectively. In this study, we combined different computational tools to extract, process and visualize the gene expression data of 25 genes across 96 regions of the adult C57Bl/6J mouse brain, implicated in glucocorticoid neurodynamics. These data derive from the anatomic gene expression atlas of the adult mouse brain of the Allen Institute for Brain Science, captured via the in situ hybridization technique. A careful interrogation of the datasets referring to these 25 genes of interest, based on a targeted, prior knowledge-driven approach, revealed useful pieces of information on spatial differences in the glucocorticoidsensitive receptors, in the regional capacity for local glucocorticoid biosynthesis, excretion, conversion to other biologically active forms and degradation. These data support the importance of the corticolimbic system of the mammalian brain in mediating glucocorticoid effects, and particularly hippocampus, as well as the need for intensifying the research efforts on the hormonal role in sensory processing, executive control function, its interplay with brainderived neurotrophic factor and the molecular basis for the regional susceptibility of the brain to states of prolonged high hormonal levels. Future work could expand this methodology by exploiting Allen Institute's databases from other species, introducing complex tools of data analysis and combined analysis of different sources of biological datasets.