Long-term or short-term corticosterone treatment suppresses adult hippocampal neurogenesis leading to anxiety-like behaviors and cognitive deficits by activating autophagy and depleting Brain-derived neurotrophic factor (BDNF)

Autophagy is regarded as a self-protective procedure of cells, however, it can also cause the death of cells under certain conditions and thereby cause the death of neural stem cels and lead to cognitive deficits. Previous studies hold different opinions of the way autophagy leads to cognitive deficits. One opinion is that corticosterone directly (CORT) directly surpasses AHN and lead to anxiety-like behaviors and cognitive deficits, another opinion is that CORT treatment causes the depleting of BDNF, and thereby lead to anxiety-like behavior and cognitive deficits. In our study, we conducted several behavioral tests on mice with short-term and long-term corticosterone treatment to determine the reason of the death of neural stem cells, in both short-term and long-term corticosterone treatments, the mice are injected with corticosterone, AAV, and BrdU regularly, and our conclusion is that in short-term treatment, it is the decline of BDNF that cause cell death, while in long-term treatment, both the decline of BDNF and autophagy itself contribute to cell death..