Erasure of fear memory is thought to be a therapeutic target for emotional disorders such as post-traumatic stress disorders (PTSD). Memantine (MEM) is a noncompetitive N-methyl-D-aspartate (NMDA) glutamate receptor antagonist and has known to enable to increase in adult hippocampal neurogenesis. Our previous study has shown that increasing adult hippocampal neurogenesis enhanced forgetting of hippocampus-dependent memory formed recently. In this study, we tried to examine effects of MEM treatment on forgetting of hippocampus-dependent fear memory. Mice were contextual fear-conditioned with an electrical footshock and then received systemic injections of MEM (50 mg/kg body weight) once a week for 4 weeks. We found that MEM-treated group displayed disruption of contextual fear memory following the MEM treatment, while control group treated with saline displayed normal contextual fear memory. Importantly, MEM-treated group did not show spontaneous recovery of fear memory even a month after the MEM treatment. Moreover, we observed similar effects of MEM treatment on inhibitory avoidance memory, another type of hippocampus-dependent fear memory. In contrast, MEM-treated group showed normal amygdala-dependent cued fear memory. Interestingly, there was a significant negative correlation between the number of neurons increased by MEM and differences of freezing scores before and after the MEM treatment in contextual fear conditioning task. These observations suggest that MEM treatment enables to erase hippocampus-dependent fear memory by enhancing memory forgetting through the increase in adult hippocampal neurogenesis. Thus our findings suggest a possible therapeutic treatment to weaken traumatic memory. We are now examining effects of the MEM treatment on remote fear memory.