Empathy has been considered a high-level cognitive process that is expressed exclusively by humans; however, recent evidence has revealed empathy-based behaviors in rodents. The rodent models provide experimental platforms to investigate the neural basis that brings about empathy and help elucidating the mechanisms underlying pathological conditions, such as autism spectrum disorders (ASDs). People with ASD have social impairments and often lack the ability to fully understand emotions in others. We developed a fear observational system in which a mouse (observer) exhibits freezing behavior through observation of another freezing mouse that receives repetitive foot shocks (demonstrator). We found that the freezing of observers was enhanced when they had received a priming foot shock, suggesting that empathy is facilitated by a commonly shared experience. We then investigated empathetic behavior in ASD model mice. The ASD model was produced by intraperitoneal injection of poly(I:C) into pregnant females. In poly(I:C) mice, observational fear was not enhanced by a priming foot shook. This deficit is consistent with a symptom of human ASD patients. Next, we examined the pharmacological responsiveness of this emotion-driven behavior, by focusing on oxytocin, which has broad effects on social behaviors in humans as well as rodents. Intraperitoneal injection of L-368,899, an oxytocin receptor antagonist, 30 min prior to fear observation attenuated the freezing response. Thus, oxytocin is likely to mediate the empathetic behaviors of fear-observing mice. These findings provide insight into our understanding of the neural mechanisms of empathy and the development of therapeutic treatment of ASD.