Our investigation delves into the intricate interplay between adult hippocampal neurogenesis, a pivotal constituent of long-term memory, and its susceptibility to stress. The ongoing hypothesis is that stress, by impeding neurogenesis, contributes to symptoms associated with post-traumatic stress disorder (PTSD). Our work explores the potential of delta-9-tetrahydrocannabinol (THC), the psychoactive constituent of cannabis, in mitigating stress-induced gene expression alterations in astrocytes, thereby fostering neurogenesis. The initial phase involves inducing cellular stress in an astrocyte-derived glioblastoma cell line, followed by subjecting primary hippocampal mouse astrocytes to psychological stress conditions. Throughout, THC's capacity to modulate astrocytic stress responses and bolster neurons during neurogenesis is under scrutiny. During our experiments, astrocyte-derived cell lines are stressed via serum deprivation, while psychological stress in primary cells is simulated using dexamethasone treatments. Stress responses are gauged through gene expression analysis and immunostaining. We assess gene expression using real-time quantitative PCR on various relevant gene players. Preliminary findings suggest that THC amplifies the viability of stressed astrocyte-derived glioblastoma cells while leaving non-stressed cells unaffected. Moreover, THC-treated stressed cells exhibit elevated expression of BDNF and reduced levels of FGF2, compared to their non-stressed counterparts. These outcomes imply a targeted influence of THC on neurogenesis, hinting a potential specificity to certain stages of the process. Further results, involving the induction of psychological stress conditions in primary mouse astrocytes, are expected to elucidate THC's mechanisms of action and its role in supporting astrocyte-mediated neurogenesis. This comprehensive understanding holds promise for shedding light on THC's therapeutic potential in addressing stress-related disorders.