Stress-induced alterations in cognitive functions are documented to be mediated by corticosteroid hormones and hence mineralocorticoid (MR) and/or glucocorticoid receptor (GR) activation. Moreover, recent evidence underscores the pivotal role of the endocannabinoid system (ECS) as a modulator of stress responses including the impact of corticosteroids on diverse memory processes. However, the precise mechanisms governing corticosteroid-induced impairment of novel object recognition (NOR) retrieval are yet unknown. The present study aims at elucidating the intricate interactions between corticosteroids and the ECS influencing cellular functions and disrupting NOR retrieval in mice. To directly study the mechanisms of corticosterone-action on NOR retrieval, mice are injected with an NOR-impairing-dose of corticosterone (10 mg/kg) 30 min before the test session. By means of pharmacological blockade and genetic deletion of MRs in the hippocampus, our findings pinpoint the involvement of MRs, rather than GRs, located in hippocampal glutamatergic neurons. Focusing on endocannabinoid signaling, using conditional mouse mutants for CB1, in vivo fiber photometry, and in vitro organotypic hippocampal slices our recent observations suggest that the impairing effect of corticosterone on NOR retrieval necessitates mtCB1 receptors and involves a dysregulation of mitochondrial and cytosolic calcium dynamics in hippocampal GABAergic interneurons. These findings reveal novel insights into the mechanisms underlying the effects of corticosteroids on NOR retrieval, implicating hippocampal MRs, mtCB1 receptors, and calcium signaling. Overall, our work introduces new elements to the understanding of how corticosteroids and the ESC intricately interact to mediate cognitive consequences of stress.