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The effects of hippocampal (HPC) damage on rats’ novel object preference (NOP) performance have been rather consistent, in that HPC lesions do not disrupt novelty preferences on the test. Conversely, there have been inconsistent findings regarding the effects of perirhinal cortex (PRh) lesions on rats’ novel-object preferences. Given the concerns that have been raised regarding the internal validity of the NOP test, viz. that the magnitude of the novel-object preference does not necessarily reflect the strength in memory for an object, it could explain the discrepant findings. The goal of the present experiment was to examine the effects of PRh and HPC lesions on rats’ object-recognition memory using a new modified delayed nonmatching-to-sample (mDNMS) task, as it circumvents the interpretational problems associated with the NOP test. Rats received PRh, HPC, or Sham lesions and were trained on the mDNMS task using a short delay (∼30 s). Both PRh and HPC rats acquired the task at the same rate as Sham rats, and reached a similar level of accuracy, indicating intact object-recognition. Thereafter, rats were tested on the NOP test using a 180-s delay. Rats with HPC lesions exhibited significant novel-object preferences, however, both the PRh and Sham rats failed to show a novelty preference. The discrepancy in both the PRh and Sham rats’ performance on the mDNMS task and NOP test raises concerns regarding the internal validity of the NOP test, in that the magnitude of a rat’s novel-object preference does not accurately reflect the persistence or accuracy of a rat’s memory for the sample object.

Damage to the perirhinal cortex (PRh) in rats impairs anterograde object-recognition memory after retention intervals of up to several hours, but there is little direct evidence to link PRh function to object-recognition abilities after substantially longer intervals that span several days or weeks. We assessed the effects of PRh lesions on anterograde object recognition using a novel-object preference test, with retention intervals lasting 24 h and 3 weeks. The rats received multiple exposures to the sample object during the learning phase--5 min per day on 5 consecutive days. Control rats displayed a significant novel-object preference after both retention intervals, indicating recognition of the sample object, whereas the rats with PRh lesions displayed a significant preference after the 24-h interval, but not after the 3-week interval. When the learning phase of the trial was shortened to a single 5-min session, the PRh group was impaired in the 24-h condition. The findings indicate that the disruptive effects of PRh damage on anterograde object recognition persist over very long postlearning intervals. The results indicate further that object recognition impairments following PRh damage are not ubiquitous, and that learning conditions play a significant role in determining the subsequent recognition performance in rats with PRh damage.

Object recognition memory was assessed on a novel-object preference (NOP) task in rats with lesions of the hippocampal formation (HPC). The learning and test phases of NOP trials occurred in either the same context or in different contexts. When the learning and test contexts were the same, rats with HPC lesions performed like control rats, displaying a significant tendency to investigate a novel object more than a familiar sample object. When the test occurred in a context that was familiar but different from the learning context, performance was unaffected in control rats, but rats with HPC lesions no longer discriminated between the objects, and therefore showed no evidence of recognizing the sample object. When the test context was unfamiliar, novel-object preference in control rats was attenuated but still above chance levels, whereas rats with HPC lesions did not show a preference. The data suggest that the HPC is not critical for encoding or retrieving conjunctive representations of the context in which incidental learning occurs, whereas it plays an essential role in recognition of objects that are subsequently encountered in different contexts.

Oxytocin has been previously associated with social attachment behaviors in various species, however, most studies focused on partner preference in the socially-monogamous prairie vole. In these, oxytocin treatment was shown to promote partner preference, such that females receiving either central or pulsatile peripheral administration would spend more time with a familiar male. This behavioral outcome was blocked by oxytocin receptor antagonist treatment. The aim of the current study was to further explore the preference-inducing properties of oxytocin by examining its effects on object preference on ovariectomized female rats. In other words, we assessed whether these effects would apply to objects and if they would be persistent across species. Eight rats were infused with oxytocin into the left ventricle and object preference was assessed at two delays: 30 min and 4 h. At the 30 min delay, oxytocin-treated animals showed preference for the familiar object, whereas saline-treated controls exhibited preference for the novel object. At the 4 h delay, both groups showed novel-object preference. Our findings show that oxytocin modulates object preference in the female rat at a shorter delay, similar to the findings from partner-preference studies in the prairie vole, suggesting that the mechanisms driving object preference might be in part similar to those responsible for partner preference.

Three experiments examined the effects of perirhinal cortex lesions on rats' retrograde and anterograde memory for object-discriminations and water-maze place-memory problems. In Experiment 1, rats learned two object-discriminations - the first was learned 2 weeks before surgery and the second 24 h before surgery. Rats with perirhinal cortex lesions displayed mildly impaired retention of both object discriminations, with no evidence of a temporal gradient. They also learned a new discrimination at a normal rate, but were impaired on a retention test 24 h later. In Experiment 2, rats learned two water-maze place problems, conducted in different rooms - the first was learned 4 weeks before surgery and the second during the week immediately before surgery. Rats with perirhinal cortex lesions displayed deficits on the early retention trials of both place problems, but they quickly relearned both problems. In Experiment 3, rats with perirhinal cortex lesions learned a new place problem at a normal rate and performed as well as control rats on a retention test 3 weeks later. Although some of the results are consistent with the conclusion that perirhinal damage disrupts storage or retrieval of place information acquired before surgery, additional considerations suggest instead a role for perirhinal cortex in the representation of nonspatial information that makes a useful but nonessential contribution to water-maze performance.

We investigated whether the ventral and dorsal hippocampus were differentially involved in incidental spatial learning. Rats with ventral and dorsal hippocampal lesions were tested on an unreinforced test of spatial memory that takes advantage of their natural propensity to explore novelty. Rats were presented with two copies of an identical object in a large circular open field arena. Subsequently, the rats were placed back into the open field with one of the objects displaced to an adjacent quadrant of the arena. Sham-operated rats and rats with ventral hippocampal lesions spent more time in the quadrant that contained the displaced object than in the quadrant that contained the non-displaced object, and more time investigating the displaced object than the non-displaced object. Rats with dorsal hippocampal lesions were impaired on both measures. Both sham and ventral hippocampal lesioned rats subsequently learned to retrieve a food pellet in the ends of each arm of a radial maze. Rats with lesions to the dorsal hippocampus showed no significant improvement in the number of errors made across training sessions and made significantly more errors, overall, than rats with ventral hippocampal or sham lesions. The findings suggest that an intact dorsal but not ventral hippocampus is necessary for spatial learning in rats.

Two experiments examined the contribution of the perirhinal cortex (PRh) to retrograde memory for the location of a platform in a water maze. In a previous study, we found that electrolytic lesions of the PRh produced retrograde amnesia, without a temporal gradient, for water-maze problems acquired 4 weeks and 2 days before surgery [Behav. Brain. Res. 114 (2000) 119]. In Experiment 1, we used the same mixed design as in our previous report (time of learning was a within-subjects factor), but PRh lesions were made by aspiration. Contrary to our earlier report, these PRh rats displayed good retention of both platform locations. Combined, these findings indicate that the lesion method may contribute importantly to the pattern of deficits observed. Experiment 2 was conducted similar to Experiment 1, except that a completely between-subjects design was used (time of learning was a between-subjects factor). Rats that received PRh lesions approximately 2 days after the last training session displayed impaired retention of the platform’s location, whereas rats that received PRh lesions 4 weeks after training did not. This finding of a temporally graded retrograde amnesia is consistent with our earlier report, and further suggests that the involvement of the PRh in the retention of water-maze problems is time-limited. However, also consistent with our earlier report, the PRh-lesioned rats in Experiment 2 that displayed a retention deficit rapidly reacquired the task. This finding, combined with the negative findings in Experiment 1, suggests that the contribution of the PRh to retrograde memory for platform locations is subtle and may not be due to impaired spatial memory abilities. Additionally, the conflicting results of Experiments 1 and 2 underscore the importance of the design employed in studies of retrograde amnesia in animals.

This experiment examined the effects of perirhinal cortex (PeRh) lesions on rats' retrograde memory for object-discriminations and retrograde object recognition. Rats learned one discrimination problem or five concurrent discrimination problems 4 weeks before surgery, and a new problem or five new problems during the week preceding surgery. Each rat was also familiarized with a sample object in an open field, 5, 3, or 1 week before surgery. PeRh-lesioned rats displayed normal retention of the object discrimination problems, but on a test of novelty preference they showed evidence of impaired recognition of the sample objects. A similar dissociation was observed on anterograde tests of object-discrimination learning and object recognition. The findings suggest the perirhinal cortex plays an essential role in rats' ability to discriminate the familiarity of objects previously encountered either before or after surgery, but this ability may not be essential for accurate performance of a simple object-discrimination task.

One of the routine memory abilities impaired in amnesic patients with temporal-lobe damage is object-recognition memory--the ability to discriminate the familiarity of previously encountered objects. Reproducing this impairment has played a central role in animal models of amnesia during the past two decades, and until recent years most of the emphasis was on describing how hippocampal damage could impair object recognition. Today most investigators are looking outside the hippocampus to explain the impairment. This paper reviews studies of object-recognition memory in rats with hippocampal damage produced by ablation, fornix transection, or forebrain ischemia. Some new perspectives on previous findings reinforce the conclusion that damage to the hippocampus has little if any impact on the ability to recognize objects, while damage in some areas outside the hippocampus is far more effective. The few circumstances in which hippocampal damage can impair performance on object-recognition tasks are situations where ancillary abilities are likely to play a significant role in supporting task performance. Some of the factors that contributed to the origins and persistence of the hippocampalcentric view of object-recognition are considered, including lesion confounds, failure to distinguish between impaired task performance and impairment of a memory ability, and disproportionate attention to a few lesion studies in monkeys, even though the hypothesis was tested far more times in rats, under a greater variety of conditions, and rejected on nearly every occasion.

Using a within-subjects design, rats were trained on two place-memory problems and five object-discrimination problems at different intervals prior to receiving either ibotenate lesions of the hippocampal formation or sham surgery. Places c 1 and 2 were fixed-platform water-maze tasks that were run in different rooms and they were learned during the 14th and 2nd week before surgery, respectively. Object-discrimination problems c 1‐5 were learned during the 13th, 10th, 7th, 4th, and 1st week before surgery, respectively. Rats with hippocampal lesions displayed impaired retention of both Place problems with no evidence of a temporal gradient to the impairment. In contrast to their retrograde place-memory deficits, the hippocampal rats displayed normal retention of the five object-discriminations that were learned before surgery. Hippocampal lesions had similar consequences for anterograde learning, as the lesioned rats were impaired in acquisition of a new water-maze problem that was run in a third room (Place c3), whereas they showed normal acquisition of two new object-discriminations. The findings indicate that the hippocampal formation is not required for long-term consolidation of information underlying accurate performance of object-discriminations, and that its critical role in memory for places persists for at least 14 weeks, and probably for as long as those memories exist. © 1999 Elsevier Science B.V. All rights reserved.

Rats behaviorally anticipate a fixed, daily opportunity to feed by entrainment of circadian oscillators that are physically separate from the light-entrainable circadian pacemaker that has been localized to the suprachiasmatic nucleus. Neural substrates mediating food-entrained rhythms are unknown. A variety of anatomical and functional observations suggest possible involvement of the limbic system and its dopaminergic component in the regulation of these rhythms. To test this hypothesis, the activity rhythms of rats bearing large, combined ablations of the hippocampus and amygdala or nucleus accumbens and medical forebrain anterior to the thalamus were examined under ad-lib feeding, 2 h daily feeding, and total food deprivation conditions. Some hippocampal-ablated rats showed alterations of free-running rhythms under ad-lib feeding, but none of the ablations impaired the rats' ability to anticipate daily feeding, or 'remember' the phase of feeding time during subsequent food deprivation. Additional groups of intact rats were treated with the dopamine antagonist haloperidol (0.3 mg/kg or 2.0 mg/kg) 30 min prior to daily feeding, but this also did not prevent the emergence of food-entrained rhythms. The limbic and dopamine systems do not appear to play a necessary role in the generation or entrainment of food-anticipatory circadian rhythms.