In a new rat model of obsessive–compulsive disorder (OCD), ‘compulsive’ behaviour is induced by attenuating a signal indicating that a lever‐press response was effective in producing food. We have recently found that compulsive lever pressing is increased following lesions to the rat orbital cortex, in accordance with several lines of evidence implicating the orbitofrontal cortex in the pathophysiology of OCD. In view of the functional similarities between the orbital cortex, the basolateral nucleus of the amygdala and the medial prefrontal cortex, the present study compared the effects of lesions to these three regions. The present study replicated the finding that lesions to the rat orbital cortex enhance compulsive lever pressing. In contrast, lesions to the dorsal medial prefrontal cortex and to the basolateral amygdala did not affect compulsive lever pressing. A comparison of these findings to current knowledge regarding similarities and differences in the functioning of the three regions sheds light on the mechanism by which signal attenuation induces compulsive lever pressing and on the role played by the orbital cortex in compulsive behaviour.