Male hooded rats received either a medial septal lesion or a control operation. The rats were then tested on an operant go/no-go discrimination task, first without a delay contingency (20 days), followed by 25 days under an 8-s delay. A discrete trial procedure with symmetrical reinforcement was used. Each trial began with the operant chamber darkened, except for back illumination of a centrally located press panel. Depression of this panel extinguished the back light and initiated a random presentation of either the go stimulus (2800 Hz tone) or the no-go stimulus (10 Hz pulsing light) for 3 s. Stimulus termination initiated the appropriate delay contingency (0 s or 8 s), which was followed by the cued availability of a lever for 2 s. If the rat pressed the lever on go trials, or refrained from pressing the lever on no-go trials, a food pellet was delivered. The data (% correct responses) were averaged over 5-day blocks. Overall, the septal-lesioned rats performed significantly better than the control rats under both 0-s delay (p < 0.025) and 8-s delay (p < 0.001) contingencies. Although there was not a significant difference between the groups during the last block of the 0-s delay (septals 93% correct, controls 89% correct, p > 0.05) or the first block of the 8-s delay (septals 54% correct, controls 53% correct, p > 0.05), the septal-lesioned animals performed significantly better than the controls during all the remaining phases of the experiment. For example, during the final 5-day block of the 8-s delay, the septal-lesioned rats averaged 71% correct and the control rats averaged 61% correct (p < 0.001). The results support the hypothesis that damage to the septal area produces a deficit in response memory which, in turn, induces a compensatory enhancement of stimulus memory.