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CO 2 inhalation can provoke panic attacks in humans, and the likelihood is increased in patients with panic disorder. Identifying brain sites involved could provide important mechanistic insight into the illness. In mice, the amygdala has been suggested to promote CO 2 responses; however, recent studies in humans with amygdala damage indicate the amygdala is not required for CO 2 -induced fear and panic and might actually oppose these responses. To clarify the role of the amygdala, we produced lesions in mice paralleling the human lesions, and characterized behavioral responses to CO 2 . Compared to sham controls, we found that amygdala-lesioned mice froze less to 10% CO 2 , and unlike shams they also began to jump frenetically. At 20% CO 2 , controls also exhibited jumping, suggesting it is a normal response to more extreme CO 2 concentrations. The effect of amygdala lesions was specific to CO 2 as amygdala-lesioned mice did not jump in response to a predator odor or to an auditory conditioned stimulus. In amygdala-lesioned mice, jumping evoked by 10% CO 2 was eliminated by co-lesioning the dorsal periaqueductal gray, a structure implicated in panic and escape-related behaviors. Together, these observations suggest a dual role for the amygdala in the CO 2 response: promoting CO 2 -induced freezing, and opposing CO 2 -induced jumping, which may help explain the exaggerated CO 2 responses in humans with amygdala lesions., (Published by Elsevier B.V.)