The aim of this study was to examine the role of the sublenticular extended amygdala (SEA) in processes of reward and reinforcement. Previous studies have examined the effects of ibotenate lesions in this area on motivation for cocaine reward. In this study, animals were trained to work for sucrose pellets, rather than a drug, on a progressive-ratio schedule of reinforcement. Bilateral intracerebral infusions of ibotenic acid (lesion group) or vehicle (control group) were made into the SEA, following the same procedures as used in previous studies. After recovery from surgery, animals were tested for six sessions on the progressive ratio schedule. The lesion did not result in motivational impairments of the kind that have previously been reported: rather than decreases in breaking point (a measure of motivational strength), the lesion resulted in greater variability of breaking points, with a tendency for lesioned animals to work harder for reward than controls. The SEA-lesioned rats did not show the increase in postreinforcement pause that usually accompanies the increase in perceived work as the number of bar presses for a reward increases. Histological analyses showed that the ibotenate lesions had successfully destroyed the SEA and that damage was also present in adjacent structures. The results are interpreted in terms of a mnemonic, rather than a motivational, deficit.