The effects on the expression of conditioned bradycardia of pairing an early (fourth postnatal day) cerebellar vermal lesion with a lesion of the medial prefrontal cortex (mPFC) were studied in adult New Zealand rabbits. In the conditioning procedure, an auditory stimulus (5 s, 1000 Hz) served as a conditioning stimulus (CS) and a train of electrical impulses applied to the ear (500 ms, 100 Hz, 1.5 mA) was used as the unconditioned stimulus (US). Heart rate (HR) responses exhibited by rabbits with the early double lesion (PFCBs) during orientation (CS-alone) and conditioning (CS-US paired) were analyzed and compared with those shown by unoperated controls as well as by a group of animals in which a cerebellar lesion alone had been performed on the fourth postnatal day (CBs). In all the experimental groups vermal lesions were localized in the cortex of lobules V-VII and the underlying white matter. As for mPFC ablation, the lesioned area involved the agranular precentral region (Brodmann's area 8), the anterior cingulate cortex (Brodmann's area 24) and the prelimbic area (Brodmann's area 32). All the experimental animals had a normal baseline HR as well as a marked orientation response, both comparable with those exhibited by controls. In contrast, while CB rabbits showed an increase in the amplitude of the conditioned bradycardic response when compared with controls, the HR conditioned response of PFCB animals was comparable to that exhibited by controls. These results suggest that, since the double lesion produces a conditioned bradycardia similar to that of the controls, the increase in the amplitude of this response observed after early cerebellar removal may depend on the mPFC which, in the absence of specific cerebellar circuits, is unable to produce a properly calibrated HR conditioned response.