The dorsal portion of the periaqueductal Gray (DPAG) is notably associated with defensive behavior and panic attacks in humans. Electrical stimulation of the DPAG induces a repertoire of defense: dPAG-evoked freezing, escape reaction and dPAG post-stimulation freezing. Past evidence support the hypothesis that whereas dPAG-evoked freezing would serve as model of panic attack, the dPAG post-stimulation freezing appears to be a model of panic disorder. The experiment 1 used two lines of animals selectively bred for high (Carioca High-Freezing) and low (Carioca Low-Freezing) freezing in response to contextual cues associated with footshock. The results suggest that although anticipatory anxiety might exert an inhibitory effect on the dPAG-evoked freezing and escape reaction, it might also facilitate the dPAG post-stimulation freezing. The experiment 2 studied the effect of electrolytic lesions on rostral anterior cingulated cortex (rACC). The results of electrolytic lesions on rACC suggest that although rACC lesions did not change the dPAG-evoked freezing and escape threshold, it might exert an inhibitory effect on the dPAG post-stimulation freezing, reinforcing the hypothesis that dPAG-evoked freezing and dPAG post- stimulation freezing are modulated by two independent circuitry of defense. The experiment 3 studied pain sensibility of rACC lesioned animals submitted to formalin test on conditioned analgesia paradigm. The results suggest that rACC lesions might exert an inhibitory effect on conditioned analgesia and consequently exacerbates recuperative behavior. The results also support the hypothesis of the rule of rACC on pain modulation.