The effects of ibotenate lesions of the hippocampus (HIPP) or hippocampus plus collateral damage to extrahippocampal structures (HCX) were investigated in rats trained to criterion on spatial versions of either a delayed-match (DMS) or delayednonmatch-to-sample (DNMS) task. After recovery from surgery, animals were retrained at "0" sec delays, then assessed at 0-30 sec delays for 15 d, retrained again at 0 sec delays, and retested for another 25 d on 0-30 sec delays. Pretrained HIPPlesioned animals showed marked delay-dependent deficits in both tasks that never recovered. Detailed examination of within-and between-trial performance factors, including changes in response preferences, length of previous trial delay, and sequential dependencies, revealed important factors operating in lesioned animals that were either absent or insignificant before the lesion. Pretrained HCX-lesioned animals showed deficits similar to those of HIPP animals, with the noticeable exception of a strong "recency" influence of the previous trial. Another group of HIPP-and HCX-lesioned animals trained on the tasks after the lesion showed reduced impairments of the type described above, suggesting that extrahippocampal structures trained after the lesion can assume the role of the hippocampus to some degree. The findings indicate that both the type of lesion and the previous history of the animal determine the postlesion DMS and DNMS performance of animals suffering damage to the hippocampus and/or related structures.
Key words: ibotenate lesion; hippocampus; subiculum; entorhinal cortex; delay tasks; memory; trainingThe effects of hippocampal lesions on delayed-match (DMS) and delayed-nonmatch-to-sample (DNMS) performance have historically provided evidence of selective influences on short-versus long-term memory processes (Correll and Scoville, 1965;Olton and Feustle, 1981;Rawlins, 1985;Parkinson et al., 1988;Raffaele and Olton, 1988;Z ola-Morgan et al., 1993;Shaw and Aggleton, 1995). In recent years the validity of this assumption has been repeatedly tested with respect to the species of animal (Aggleton and Mishkin, 1985;Rothblat and Kromer, 1991;Gaffan and Murray, 1992;Rawlins et al., 1993), type of delay task used, (Parkinson et al., 1988;Dunnett, 1989;Rothblat and Kromer, 1991;Rawlins et al., 1993;Steele and Rawlins, 1993;Cassaday and Rawlins, 1995), number of choices available (Angeli et al., 1993;Gutnikov et al., 1994), type and extent of the lesion (Aggleton and Mishkin, 1985;Aggleton et al., 1989;Jarrard, 1989Jarrard, , 1993Coffey et al., 1990;Rawlins et al., 1993), nature of stimuli used (Angeli et al., 1993;Yee and Rawlins, 1994; C assaday and Rawlins, 1995), and methods of scoring the data (Ringo, 1991;Steele and Rawlins, 1993).Several of these issues can be reduced to four important aspects of DMS and DNMS behavior that have yet to be unequivocally determined in animals that have damage to the hippocampus and related structures. The first is whether the deficit in DMS and DNMS performance reported with lesions of the hippoca...