Stress-related psychiatric disorders have been associated with polymorphisms in the gene encoding FK506-binding protein 5(FKBP5), a co-chaperone of the glucocorticoid receptor(GR). Stress response is coordinated by the hypothalamic-pituitary-adrenal(HPA) axis, through secretion of glucocorticoids(GC). Additionally, the HPA is a site of convergence of the circadian clock and the stress response systems. Physiologically, GCs act as molecular effectors of circadian rhythm that synchronize transcriptional and metabolic activity in peripheral tissues. However, not much is understood about the analogous regulation in the brain. We have previously shown that astrocytes are a cellular target of GR-dependent transcriptional activity in the brain, and that this signaling contributes to the central stress response. The goal of this study was to test whether GR control of clock gene oscillations in astrocytes relies on Fkbp5. Quantitative polymerase chain reaction(qPCR) was used to measure the expression levels of clock genes and bona fide GR targets in primary astrocyte cells from both the wild-type and Fkbp5 knockout model treated with GR agonist, 100 nM dexamethasone(DEX). Furthermore, state-of-the-art long term live imaging of genetically encoded fluorescent reporters was used to visualize selected clock gene oscillatory activity. We observed that GR stimulation reliably elicited oscillations of clock genes with a period of approximately 26h, independent of the reporter and genotype. However, Fkbp5 knockout differentially affected the amplitude of Cry1 and Bmal1 oscillations beyond the first cycle. We conclude that Fkbp5 moderates GR-dependent regulation of clock genes in astrocytes. The new toolbox allows to explore circadian biology of human and mouse neural cells.