Re-exposure to the conditioned stimulus (CS) during which the threat was experienced leads to two different processes: brief CS presentation initiates reconsolidation to re-stabilize the original fear memory, whereas prolonged CS presentation leads to extinction to form an inhibitory memory. The two processes used distinct mechanisms, but the difference in neuronal activation during these processes still remains to be addressed. Using the auditory fear-conditioning model, we analyzed Arc (activity-regulated cytoskeletal-associated protein) expression after brief or prolonged CS presentation at several time points. Here, we reported that Arc expression increased in the amygdala and infralimbic prefrontal cortex from 2 to 6 h after 20 trials of CS presentation, whereas the Arc expression increased mainly in the basolateral amygdala (BLA) 2 h after one trial of CS presentation. The Arc+ neurons in BLA induced by brief or prolonged CS presentation were non-GABAergic, suggesting that the activation of the non-GABAergic neurons in BLA might be involved in memory reconsolidation and extinction processes of the auditory fear condition. Our results also suggest that memory reconsolidation or extinction of auditory fear conditioning induced Arc activation in distinct neural circuits.