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Recognition memory, the discrimination of a novel from a familiar event, can be classified into item recognition and associative recognition. Item recognition concerns the identification of novel individual stimuli, while associative recognition concerns the detection of novelty that arises when familiar items are reconfigured in a novel manner. Experiments in rodents that have mapped the expression of immediate-early genes, e.g., c-fos, highlight key differences between these two forms of recognition memory. Visual item novelty is consistently linked to increased c-fos activity in just two brain sites, the perirhinal cortex and the adjacent visual association area Te2. Typically there are no hippocampal c-fos changes. In contrast, visual associative recognition is consistently linked to c-fos activity changes in the hippocampus, but not the perirhinal cortex. The lack of a c-fos perirhinal change with associative recognition presumably reflects the fact that the individual items in an array remain familiar, even though their combinations are unique. Those exceptions, when item recognition is associated with hippocampal c-fos changes, occur when rats actively explore novel objects. The increased engagement with objects will involve multisensory stimulus processing and potentially create conditions in which rats can readily learn stimulus attributes such as object location or object order, i.e., attributes involved in associative recognition. Correlations based on levels of immediate-early gene expression in the temporal lobe indicate that actively exploring novel stimuli switches patterns of entorhinal-hippocampal functional connectivity to emphasise direct entorhinal-dentate gyrus processing. These gene activity findings help to distinguish models of medial temporal lobe function.

Bilateral damage in the posterior cingulate region can induce anterograde amnesia. Identifying the potential contributions of the various areas within this heterogeneous region has, however, largely depended on animal research. Within the posterior cingulate region the retrosplenial cortex stands out by virtue of its dense interconnections with the hippocampal formation and anterior thalamic nuclei. Consistent with these connections is the finding from lesion studies in animals that the retrosplenial cortex is necessary for navigation and spatial learning, and that these functions occur in close conjunction with the hippocampal formation and anterior thalamus. Suggested functions include the creation and maintenance of scenes, linked to the switching between scenes based on different frameworks (e.g. egocentric versus allocentric). More fine-grain analyses suggest that there are functional distinctions between the subregions within the retrosplenial cortex, though these subregions are likely to then act as a coordinated unit. Other studies reveal that the retrosplenial cortex is highly sensitive to damage in distal sites, including damage to sites that do not have direct retrosplenial connections. The resultant retrosplenial dysfunctions, which include decreases in metabolic activity and a loss of plasticity, may contribute both to diencephalic and temporal lobe amnesias as well as to Alzheimer's disease.

Forced-choice tests of recognition have become the favoured behavioural method for the assessment of models of amnesia in nonhuman primates, yet the profile of deficits shown by human amnesic subjects remains uncertain. The present study explored the performance of 12 amnesic subjects on two delayed matching-to-sample tasks. Experiment 1, which used retention delays of between 2 and 60 sec, confirmed that amnesia impairs such tasks, even when there is only one item to be remembered. The results also highlighted the need to match levels of performance before the effects of delay can be interpreted. In Experiment 2 care was taken to eliminate ceiling effects and to match the subjects at the shortest delay (3 sec). This was achieved by giving the control subjects harder versions of the same task. The amnesic subjects still showed a faster rate of forgetting for abstract patterns, indicating that this is a genuine feature of amnesia. In contrast, the amnesic subjects' performance on a spatial matching-to-sample task was not differentially affected by delays of up to 40 sec. There was no evidence that the amnesic subjects were disproportionately impaired on this spatial task, nor could the different aetiological groups be distinguished by their patterns of DMS performance.

Findings of pharmacological studies that have investigated the involvement of specific regions of the brain in recognition memory are reviewed. The particular emphasis of the review concerns what such studies indicate concerning the role of the perirhinal cortex in recognition memory. Most of the studies involve rats and most have investigated recognition memory for objects. Pharmacological studies provide a large body of evidence supporting the essential role of the perirhinal cortex in the acquisition, consolidation and retrieval of object recognition memory. Such studies provide increasingly detailed evidence concerning both the neurotransmitter systems and the underlying intracellular mechanisms involved in recognition memory processes. They have provided evidence in support of synaptic weakening as a major synaptic plastic process within perirhinal cortex underlying object recognition memory. They have also supplied confirmatory evidence that that there is more than one synaptic plastic process involved. The demonstrated necessity to long-term recognition memory of intracellular signalling mechanisms related to synaptic modification within perirhinal cortex establishes a central role for the region in the information storage underlying such memory. Perirhinal cortex is thereby established as an information storage site rather than solely a processing station. Pharmacological studies have also supplied new evidence concerning the detailed roles of other regions, including the hippocampus and the medial prefrontal cortex in different types of recognition memory tasks that include a spatial or temporal component. In so doing, they have also further defined the contribution of perirhinal cortex to such tasks. To date it appears that the contribution of perirhinal cortex to associative and temporal order memory reflects that in simple object recognition memory, namely that perirhinal cortex provides information concerning objects and their prior occurrence (novelty/familiarity)., Highlights ► Perirhinal cortex role in recognition memory. ► Effect of selective pharmacological interventions in specific brain regions on recognition memory. ► Impairments produced by glutamatergic & cholinergic antagonists & compounds targeting intracellular signalling mechanisms. ► Effects on object, object-in-place and temporal order recognition memory.

This paper first reviews the anatomical, pathological, and neuropsychological evidence implicating the anterior thalamic nuclei in memory processes. It is concluded that there is much indirect evidence indicating that anterior thalamic dysfunction is an important factor in anterograde amnesia. More direct evidence for the involvement of the anterior thalamic nuclei in memory processes emerges from two experiments with rats that examined performance of a spatial test of working memory, delayed nonmatching-to-position. The first study revealed that neurotoxic lesions of the anterior thalamic nuclei and radiofrequency lesions of the fornix both produce equivalent performance deficits. In contrast, lesions of the mamillary bodies were without effect. A second study showed that lesions of the fornix and removal of the hippocampus produced very similar deficits. These data indicate that while the involvement of the anterior thalamic nuclei in certain memory functions depends on inputs from the hippocampus, this involvement need not depend on indirect afferents via the mamillary bodies.

The present study examined the performance of two groups of amnesic subjects on a cross-modal identification task. It was found that subjects with Korsakoff's disease did not differ from alcoholic controls on their ability to match the tactile feel of an arc with the visual appearance of the full circle from which the arc was taken. The postencephalitic subjects were, however, impaired on this same task. All groups performed normally on two intramodal control tasks. The postencephalitic group, like the Korsakoff subjects, were also poor at identifying common objects from tactile cues. The results are consistent with the notion that limbic regions in the temporal lobe are important for cross-modal associations.

Subject KN has a persistent anterograde amnesia as a result of brain injury following meningitis in 1993. MRI scans reveal a bilateral decrease in the volume of his hippocampal region (dentate gyrus, CA1–4, subicular cortices) of approximately 45% in both the right and left hemispheres, although the volume of his perirhinal cortex appears normal. Aside from some changes to his occipital lobe and bilateral shrinkage of the amygdala, the rest of his brain appears normal on recent quantitative MRI scans. A striking feature of his memory loss is his ability to perform at normal levels on some tests of recognition, despite his consistent deficit on tests of recall. Two tests designed specifically to distinguish performance of two putative divisions of recognition memory (the Remember/Know procedure and the use of receiver operating characteristics to distinguish familiarity and recollection), provide evidence for a selective sparing of the familiarity component of recognition. The dissociation within recognition memory supports dual-process models of recognition, and also supports proposals that anatomically linked regions within the medial temporal lobe make qualitatively different contributions to recognition.

The integration of neural signals from different sensory modalities is a prerequisite for many cognitive and behavioural functions. In this study, we have mapped the functional anatomy of the integration of sensory signals across the tactile and visual modalities. Using the PET radiotracer H2(15)O, regional cerebral blood flow (rCBF) changes were measured in eight normal volunteers performing crossmodal recognition of simultaneously presented visual and tactile stimuli using a modified version of the 'arc-circle test'. Whilst intramodal matching within the visual modality led to relative rCBF increases in the visual association cortex, crossmodal matching (visual-tactile), when compared to intramodal matching, was accompanied by relative rCBF increases in the anterior cingulate cortex, inferior parietal lobules, the left dorsolateral prefrontal cortex (DLPFC) and the left claustrum/insular cortex. The pattern of brain activation is congruent with areas of heteromodal and supramodal cortex and indicates that activation of multimodal areas is required to solve the crossmodal problem.

The present study compared the recognition memory deficit in different groups of amnesics using scores from a standard test. The data, taken from a literature search, came from 33 studies reporting the performance of amnesic subjects on the recognition memory test (RMT) [77]. A total of 112 amnesic subjects were grouped according to their pathology. In addition, the analysis included subjects with schizophrenia, amygdala damage, or frontal lobe damage. Of these three nonamnesic groups, only the frontal lobe subjects were impaired on both RMT subtests, while the schizophrenics showed a disproportionate impairment for the recognition of faces. The amygdala subjects were also poor at face recognition. Among the amnesic groups, those subjects likely to have multiple sites of pathology (e.g. Korsakoff amnesics, post-encephalitics) were found to be the most impaired on the RMT. In contrast, those amnesics with more focal, limbic lesions in the hippocampus, fornix, or mamillary body region showed much milder deficits on the RMT task, some performing at normal levels. Despite their apparent sparing of recognition, the overall severity of amnesia in those subjects with limbic lesions appeared comparable to that in the remaining amnesics. These findings indicate that deficits on both subtests of the RMT are a frequent but not inevitable component of anterograde amnesia. They also point to a distinct subgroup of amnesias associated with selective damage in the hippocampus or its diencephalic targets, in which there is a relative sparing of recognition under certain test conditions.

Amnesic subjects suffering from Korsakoff's syndrome and post-viral encephalitis were assessed on their ability to estimate short temporal durations using two-quite different tasks. In the first experiment subjects were required to reproduce and estimate intervals of between 3 and 96 sec. In the second experiment subjects carried out an automated Fixed Interval task using intervals of 15 and 30 sec. On both tasks the Korsakoff group were impaired at all intervals compared to an alcoholic control group, whereas the post-encephalitic subjects were unimpaired compared to a normal control group. The results suggest that temporal estimation can be independent of memory function. There was, however, evidence of a relationship between the ability to estimate time intervals and performance on a particular test of frontal lobe function, cognitive estimation. The results are discussed in relation to these findings and to theories of temporal perception.

A group of amnesic Korsakoff subjects and a group of alcoholic controls were trained on a test of visual recognition, delayed matching-to-sample with trial unique stimuli. This test was modelled on comparable tasks used in the development of animal models of human amnesia. It was found that the Korsakoff subjects were severely impaired when the task difficulty was increased by lengthening the retention delay beyond 10 sec or by increasing the number of items intervening between sample presentation and test. The amnesic subjects were also impaired on the acquisition of a set of concurrent visual discriminations. These results bear clear similarities to those obtained from experimental amnesic syndromes in monkeys.

Monkeys with surgical lesions which removed the medial portions of the medial and anterior thalamic nuclei were markedly impaired on a test of object recognition. The same animals were able to learn visual pattern discriminations and a spatial delayed response task at a normal rate. These findings indicate that lesions in the medial thalamus produce a selective impairment in visual recognition memory in monkeys and, consequently, may provide an experimental model for human “diencephahc amnesia”.