Corticosterone administration induced anxiety and depression-like abnormal behavior, caused a decrease in the expression levels of the brain-derived neurotrophic factor and a decrease in the phosphorylation of protein kinase B (AKT), the mammalian target of rapamycin (mTOR), and, finally, a decrease in a cAMP response element binding protein (CREB) in the prefrontal cortex (PFC). This evidence concerns the gene AKT1 and depressive disorder.