The present study examined the role of the amygdaloid central nucleus (ACE) in the retention of differential pavlovian conditioning of bradycardia in rabbits. Electrodes were implanted bilaterally in ACE or in control sites just dorsal and rostral to ACE. Following recovery, animals were subjected to differential pavlovian conditioning in which one tone (CS+) was paired with periorbital shock and a second tone (CS-) was presented alone. Subsequent electrolytic lesions abolished the heart rate (HR) conditioned response (CR), yet had no effect on HR orienting response, unconditioned response, or baseline. In a follow-up experiment, corneoretinal potential (CRP) and HR were recorded. Bilateral ACE lesions profoundly attenuated or abolished the HR CR without abolishing CRP CRs. The major finding of this study is that bilateral lesions of ACE selectively attenuate the HR CR while not necessarily abolishing other CRs.