Adult hippocampal neurogenesis (AHN) is an intricate and mysterious process that is largely unexplored. Previous studies have shown adult neurogenesis can decrease and alter some levels of depression, however, no studies have shown a complete understanding with a specific example of how AHN actually mitigates and impacts depression-like behavior. This study focuses on the effect of inhibiting memory formation and potentiation in adult-born neurons (ABNs) on depression-like behavior, through the knockout of NMDA receptors (NMDARs). The experiment utilizes gene editing and site-specific recombination, along with optogenetic and fluorescent labeling. Predicted results are the expectancy to knockout NMDARs and prevent long-term potentiation coupled with correct expression of fluorescent. Assuming the mutated mice would perform worse in open-field and tail suspension tests compared with normal AHN mice. This leads to the conclusion that memory formation does help mediate depression-like behavior, which can be further reinforced and studied for future therapies.