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Contextual fear conditioning relies upon a network of cortical and subcortical structures, including the hippocampus and the retrosplenial cortex (RSC). However, the contribution of the hippocampus is parameter-dependent. For example, with "weak" training procedures, lesions of the hippocampus produce both retrograde and anterograde context amnesia. However, with "strong" training procedures (e.g., more trials and/or higher levels of footshock), lesions of the hippocampus produce retrograde context amnesia but not anterograde amnesia (Wiltgen et al., 2006). Likewise, prior studies have shown that with weak training, RSC lesions produce both retrograde and anterograde context amnesia (Keene & Bucci, 2008). The purpose of the current study was to examine the effects of RSC damage on contextual fear conditioning following strong training. In Experiment 1, lesions of the RSC resulted in both retrograde and anterograde context amnesia following strong training using the same unsignaled fear conditioning procedures described by Wiltgen et al. (2006). In Experiment 2, using a signaled fear conditioning procedure, we replicated these effects on context memory observing both retrograde and anterograde context amnesia. In contrast, there were no lesion effects on tone-fear memory. Thus, unlike lesions of the hippocampus, lesions of RSC produce both retrograde and anterograde context amnesia even when rats undergo strong fear conditioning. These findings suggest that the RSC has an essential role in contextual fear conditioning and that other systems or pathways are unable to compensate for the loss of RSC function., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Purpose: To describe a delayed severe complication of temporal lobectomy for intractable epilepsy., Method: A case of amnesia occurring 24 years after surgery is described and five similar cases from the literature reviewed., Results: Mean age at surgery (5 right) was 40 years (19-62 years), 3 female. Four of five tested had impaired visual and verbal memory preoperatively but not sufficient to contraindicate surgery. Pathology was mesial temporal sclerosis in 3, 1 cavernoma, 1 dysembryoplastic neuroepithelial tumor (DNET) and 1 normal. Postoperatively, four were seizure free 3-12 years off medication and two continued with seizures. There was no unexpected postoperative memory change until incapacitating anterograde amnesia developed 1-24 years after surgery. In five patients, including ours, this followed definite or possible status epilepticus with new mesial temporal sclerosis on the opposite side in the four that were investigated by MRI. One patient developed a glioblastoma in the opposite temporal lobe., Conclusion: Continuing or late recurrence of seizures from the remaining temporal lobe after temporal lobectomy can result in incapacitating amnesia if status epilepticus occurs. Other new lesions on the opposite side to surgery can have the same effect.

The amnesic effects of excitotoxic lesions of the rat retrosplenial cortex (RS) and hippocampus (HPC) in the spontaneous object recognition (SOR) performance were investigated. The SOR test consisted of the sample-exposure session(s) and a test session. First, to test retrograde amnesia, rats received four sample-exposure sessions within a day at 4 weeks and 1 day before the surgery, respectively. In the test sessions conducted 1 week after the surgery, both lesion groups showed a temporally ungraded retrograde amnesia. Second, to test anterograde amnesia, 1- and 4-week retention intervals were inserted between the four sample-exposure sessions and the test session. The RS-lesioned rats showed a retention interval-dependent impairment in the test sessions, while the HPC-lesioned rats showed an impairment regardless of the retention interval. Finally, to test short-term recognition memory, 5- or 30-min delay was interposed between the single sample-exposure session and the test session. Both lesion groups performed normally irrespective of the delay length. These results suggest that both the RS and HPC are important for long-term object recognition memory, but these areas have different roles in it., (Copyright © 2012 Wiley Periodicals, Inc.)

Learning and memory deficits are typically associated with damage or dysfunction of medial temporal lobe structures; however, diencephalic lesions are another common cause of severe and persistent memory deficits. We focus specifically on the thalamus and review the pathological and neuropsychological characteristics of two common causes of such damage: Korsakoff's syndrome and stroke. We then present a patient who had sustained bilateral medial thalamic infarctions that affected the medial dorsal nucleus and internal medullary lamina. This patient demonstrated the characteristic temporally graded retrograde amnesia and a profound anterograde memory (i.e., explicit memory) deficit within the context of relatively preserved implicit memory. Implications of this explicit-implicit discrepancy are discussed within the context of cognitive rehabilitation techniques that hold promise for more severely impaired patients.

Retrograde and anterograde amnesic effects of excitotoxic lesions of the rat retrosplenial cortex (RS) and hippocampus (HPC) were investigated. To test retrograde amnesia, rats were trained with two-arm place discrimination in a radial maze 4 wk and 1 d before surgery with a different arm pair, respectively. In the retention test 1 wk after surgery, both lesion groups showed temporally ungraded retrograde amnesia. To test anterograde amnesia, animals were trained after surgery to discriminate three arm pairs successively within a day, and then after interposition of 1- to 4-wk intervals, one of these pairs, respectively, was tested for retention. RS-lesioned rats could acquire these pairs of place discriminations rapidly but showed a retention interval-dependent impairment in the retention test. Conversely, HPC-lesioned rats took more sessions to acquire these pairs than did the control group, and their retention was approximately 70% of correct performance regardless of retention interval. Results suggest that RS and HPC have different roles in spatial memory and that RS is important for remote memory process.

Objective: The aim of the present study is to investigate the cumulative effects of a clinically determined course of electroconvulsive therapy (ECT) on anterograde and retrograde amnesia. In this study, mood and memory were examined in the context of a protocol driven by therapeutic response, rather than by preordained research criteria., Methods: Twenty-two patients with major depressive disorder and 18 nondepressed controls were taught a series of faces and names before the initiation of ECT, and their retention of this information was examined after the end of treatment. Anterograde (ie, new learning) and retrograde memory (ie, recall of information learned before ECT) were assessed. Eleven ECT patients underwent unilateral (UL) stimulation, and 11 had a combination of UL and bilateral stimulation. Major depressive disorder patients and nondepressed controls participants were matched according to baseline memory abilities. Unilateral and unilateral/bilateral (UB) ECT patients were matched according to baseline depression and memory abilities., Results: Treatment with ECT resulted in a dissociation between anterograde and retrograde memory; after treatment, major depressive disorder patients demonstrated significant retrograde amnesia, whereas there was no change in their anterograde memory. Unilateral and UB ECT patients performed equally well on tasks of anterograde memory. Contrary to our expectation, UB ECT was not associated with greater retrograde memory loss than was UL ECT treatment. However, a trend toward a group difference was present on 1 memory measure., Conclusions: Results of the study suggest that a clinical course of ECT is associated with isolated impairment for information learned before treatment (ie, retrograde memory), whereas there was no effect of ECT on posttreatment learning abilities (ie, anterograde memory).

We examined whether alternate systems compensate for deficient ones to process relations in amnesia. Transverse patterning (TP), a test of relating items to one another in memory, is reliably impaired in amnesia and has played a central role in testing hippocampal function. We facilitated successful TP in amnesia by providing familiar stimuli with semantically meaningful relationships. Tapping semantic knowledge allowed TP to be solved via extrahippocampal structures. Our work shows that by framing a situation as meaningful we can engage alternate neural systems to compensate for impairments., ((c) 2007 Wiley-Liss, Inc.)

Background: Several studies noted persistence of memory impairment following an episode of transient global amnesia (TGA) with standard tests., Aim: To specify long-term memory impairments in a group of patients selected with stringent criteria., Methods: Both retrograde and anterograde memory were investigated in 32 patients 13-67 months after a TGA episode with original tasks encompassing retrograde semantic memory (academic, public and personal knowledge), retrograde episodic memory (autobiographical events) and anterograde episodic memory., Results: Patients had preserved academic and public knowledge. Pathological scores were obtained in personal verbal fluency for the two most recent periods, and patients produced less autobiographical events than controls. However, when they were provided time to detail, memories were as episodic as in controls regardless of their remoteness. Anterograde episodic tasks revealed a mild but significant impairment of the capacity of re-living the condition of encoding, i.e. the moment at which words were presented., Conclusions: Patients who have suffered from an episode of TGA manifest deficits of memory focused on the retrieval of both recent semantic information and episodic memories and especially the capacity of re-living. These deficits may not result from a deterioration of memory per se but rather from difficulties in accessing memories.

AD, a 45-year-old man, presented with a severe and global anterograde amnesia following surgery for removal of a colloid cyst. Structural neuroimaging confirmed bilateral lesions to the fornix and a small lesion in the basal forebrain. Testing for remote episodic memory of autobiographical events, and for remote semantic memory of personal and public events, and of famous people, revealed that AD had a severe retrograde amnesia for autobiographical episodes that covered his entire lifetime, and a time-limited retrograde amnesia for semantic memory. Because the fornix and basal forebrain lesions disrupted major afferent and efferent pathways of the hippocampus, it was concluded that the integrity of the hippocampus and its projections are needed to retain and/or recover autobiographical memories no matter how old they are. By contrast, hippocampal contribution to semantic memory is time-limited. These findings were interpreted as consistent with Multiple Trace Theory, which holds that the hippocampal system is essential for recovering contextually rich memories no matter how old they are, but is not needed for recovering semantic memories.

Lesions restricted to the hippocampal formation and/or extended hippocampal system (hippocampal formation, fornix, mammillary bodies, and anterior thalamic nuclei) can disrupt conscious recollection in anterograde amnesia, while leaving familiarity-based memory relatively intact. Familiarity may be supported by extra-hippocampal medial temporal lobe (MTL) structures. Within-task dissociations in recognition memory best exemplify this distinction in anterograde amnesia. The authors report for the first time comparable dissociations within recognition memory in retrograde amnesia. An amnesic patient (A.D.) with bilateral fornix and septal nuclei lesions failed to recognize details pertaining to personal past events only when recollection was required, during recognition of episodic details. His intact recognition of generic and semantic details pertaining to the same events was ascribed to intact familiarity processes. Recollective processes in the controls were reflected by asymmetrical Receiver's Operating Characteristic curves, whereas the patient's Receiver's Operating Characteristic was symmetrical, suggesting that his inferior recognition performance on episodic details was reliant on familiarity processes. Anterograde and retrograde memories were equally affected, with no temporal gradient for retrograde memories. By comparison, another amnesic person (K.C.) with extensive MTL damage (involving extra-hippocampal MTL structures in addition to hippocampal and fornix lesions) had very poor recognition and no recollection of either episodic or generic/semantic details. These data suggest that the extended hippocampal system is required to support recollection for both anterograde and retrograde memories, regardless of their age.

We used a free-recall paradigm to establish a behavioral index of the retrograde and anterograde interference of emotion with episodic memory encoding. In two experiments involving 78 subjects, we show that negatively valenced items elicit retrograde amnesia, whereas positively valenced items elicit retrograde hypermnesia. These data indicate item valence is critical in determining retrograde amnesia and retrograde hypermnesia. In contrast, we show that item arousal induces an anterograde amnesic effect, consistent with the idea that a valence-evoked arousal mechanism compromises anterograde episodic encoding. Randomized double-blind administration of the beta-adrenoceptor antagonist propranolol compared with the selective norepinephrine (NE) reuptake-inhibitor reboxetine, and placebo, demonstrated that the magnitude of this emotional amnesia and hypermnesia can be upregulated and downregulated as a function of emotional arousal and central NE signaling. We conclude that a differential processing of emotional arousal and valence influences how the brain remembers and forgets.

This article explores the recall, item recognition, and associative recognition memory of patient B.E., whose pattern of retrograde amnesia was reported by Kapur and Brooks (1999; Hippocampus 9:1-8). Structural magnetic resonance imaging (MRI) has shown that B.E. has bilateral damage restricted to the hippocampus. The structural damage he had sustained was accompanied by bilateral hypoperfusion of the temporal lobe, revealed by positron emission tomography (PET), and which single photon emission computed tomography (SPECT) suggested was greater in the left than the right temporal lobe. B.E. showed a global anterograde amnesia for verbal material, but he displayed some sparing of nonverbal item recognition relative to nonverbal recall and associative recognition. His performance on an item recognition task that used the remember/know procedure and another that involved repetition of the test phase, to reduce the difference between the familiarity of the targets and foils, suggested that his relatively spared nonverbal item recognition may have been mainly supported by familiarity. This finding is consistent with the view that the anterior temporal lobe, including the perirhinal cortex, can support familiarity-based memory judgments (Brown and Bashir, 2002; Philos Trans R Soc Lond B 357:1083-1095). B.E.'s data also highlight the importance of functional as well as structural scan information for interpreting the pattern of memory deficits shown by patients with selective hippocampal structural lesions., ((c) 2004 Wiley-Liss, Inc.)

K.C. has been investigated extensively over some 20 years since a motorcycle accident left him with widespread brain damage that includes large bilateral hippocampal lesions, which caused a remarkable case of memory impairment. On standard testing, K.C.'s anterograde amnesia is as severe as that of any other case reported in the literature, including H.M. However, his ability to make use of knowledge and experiences from the time before his accident shows a sharp dissociation between semantic and episodic memory. A good deal of his general knowledge of the world, including knowledge about himself, is preserved, but he is incapable of recollecting any personally experienced events. In displaying such "episodic amnesia," which encompasses an entire lifetime of personal experiences, K.C. differs from many other amnesic cases. Here, we document for the first time the full extent of K.C.'s brain damage using MRI-based quantitative measurements. We then review the many investigations with K.C. that have contributed to our understanding not only of episodic and semantic memory but also to the development of other aspects of memory theory. These include the distinction between implicit and explicit memory, the prospect of new learning in amnesia, and the fate of recent and remote memory for autobiographical and public events, people, and spatial locations.

We carried out the first neuropsychological study of a series of patients with functional amnesia. We evaluated 10 patients, first with a neurological examination and then with three tests of anterograde amnesia and four tests of retrograde amnesia. Excluding one patient who later admitted to malingering, all patients had a significant premorbid psychiatric history and one or more possible precipitating factors for their amnesia. Eight of the 10 patients still had persistent retrograde amnesia at our last contact with them (median = 14 mo after the onset of amnesia). On tests of anterograde amnesia, the patients performed normally as a group, though some patients scored poorly on tests of verbal memory. On tests of retrograde amnesia, all patients had difficulty re-collecting well-formed autobiographical memories of specific events from their past. In contrast, patients performed as well as controls at distinguishing the names of cities from fictitious city names. On remote memory tests for past public events and famous faces, different patients exhibited different but internally consistent patterns of impaired and spared performance. The variability in the clinical and neuropsychological findings among our patients may be understood by supposing that memory performance is poor in proportion to how directly a test appears to assess a patient's common sense concept of memory. The presentation of patients with functional amnesia is as variable as humankind's concept of what memory is and how it works.

A forced-choice discrimination paradigm was used in two experiments, to evaluate retrograde and anterograde amnesia in rats after hippocampal ablation. In a within-subjects design (Experiment 1), rats were trained on a set of 10 olfactory discriminations 4 weeks before surgery and on a separate set of 10 discriminations 1 week before surgery. In a mixed design (Experiment 2), rats were trained on olfactory discriminations in one of three conditions: condition 1 (10 discriminations at 4 weeks before surgery); condition 2 (10 discriminations at 1 week before surgery); or condition 3 (10 discriminations at 4 weeks before surgery and 10 discriminations at 1 week before surgery). Discriminations in both experiments were rapidly learned, requiring 7-10 trials to reach criterion. After training, half of the rats in each condition received bilateral neurotoxic lesions of the hippocampus, and the other half received sham surgery. One week after surgery, all rats were given a retention test, consisting of a single critical trial for each discrimination. In both experiments, rats with selective hippocampal lesions exhibited preserved retention of these olfactory discriminations with no observable retention gradient. A postoperative acquisition test for two new discriminations indicated that anterograde memory was also preserved, while a postoperative test of spatial learning in the Morris water maze confirmed that the hippocampal lesions impaired spatial learning. Together, these experiments refute the contention that the hippocampus is requisite for (non-spatial) olfactory memory consolidation, storage, or access, despite the condition that the information be rapidly acquired.

Long-term amnesia is a slowly developing form of anterograde amnesia accompanied by retrograde amnesia of variable severity (Kapur, 1996; 1997) often associated with damage to the anterior temporal neocortex and epileptic seizures. The precise neural and functional deficits that underlie this condition are unknown. A patient, JL, who has this condition following a closed-head injury, is described in detail. Her injury caused bilateral anterior temporal neocortex damage that was more extensive on the left and right-sided damage to the perirhinal and orbitofrontal cortices. The hippocampus appeared to be intact bilaterally. Epilepsy developed within two years of JL's injury. Apart from her memory impairments, JL's cognitive functions, including high-level visual perception, attention, semantic memory and executive functions were well preserved. Her memory also seemed well preserved for at least 30 minutes following encoding. The one exception was the patient's relatively greater impairment at difficult visual recognition tests for which verbalization may not have been an effective strategy. This problem may have been caused by JL's right-sided perirhinal and orbitofrontal cortex damage. Her recall and recognition was clearly impaired after a three-week delay. She also showed a retrograde amnesia, which appeared to be milder than her remote post-morbid memory deficit. JL's remote memory was preserved for information first encountered in either the pre- or post-morbid period provided the information had received sufficient rehearsal over long periods of time. Her long-term amnesia may have been caused by anterior temporal neocortex damage, possibly in association with her epileptic seizures. Whether the condition is heterogeneous, involves a deficit in slow consolidation, disruption of unconsolidated memories, or blockage of maintenance or disruption of insufficiently rehearsed memories whether or not these have been slowly consolidated is discussed.

Recent functional neuroimaging studies have suggested that different neural substrates within the frontal lobes are associated with memory encoding, retrieval and monitoring. If this is the case, then it should be possible to find frontal patients with selective deficits to these processes. However, most laboratory based memory tests (e.g. Wechsler Memory Scale) require a combination of all these processes making it hard to find clear dissociations between patients. Using tests of everyday memory, this study documents a clear dissociation between a frontal patient's (JB) impaired ability to retrieve events from the anterograde period relative to spared ability to retrieve events from the retrograde period. This is consistent with specific disruption to frontal mechanisms associated with encoding which disrupts the formation of new episodic memories. The defective mechanism may be related to more general aspects of cognitive processing (e.g. selection demands), but it is unlikely to reflect damage to working memory (as assessed by the n-back task) as there is a clear dissociation between spared performance on this task and impaired performance on a comparable episodic recognition memory task.

Benzodiazepine (diazepam), triazolobenzodiazepines (brotizolam, triazolam) and platelet activating factor (PAF) antagonist (BN 52021) are administered to mice before acquisition and retrieval trials conducted using Morris water maze. Benzodiazepine has produced only anterograde amnesia and it has not produced retrograde amnesia. Triazolobenzodiazepines have produced both anterograde and retrograde amnesia. PAF antagonist (BN 52021) has only produced retrograde amnesia and it has not produced anterograde amnesia. The anterograde amnesia produced by benzodiazepine and triazolobenzodiazepines, has been prevented by benzodiazepine receptor antagonist (flumazenil). It suggests that benzodiazepine- and triazolobenzodiazepines-induced anterograde amnesia may be mediated through benzodiazepine receptors. On the other hand, retrograde amnesia produced by PAF antagonist (BN 52021) and triazolobenzodiazepines has been attenuated by PAF and PAF acetyl hydrolase inhibitors such as cigarette smoke extract (CSE) and phenylmethanesulfonylflouride. It suggests that triazolobenzodiazepine-induced retrograde amnesia may be mediated through blockade of PAF receptors.

It has been unclear whether the hippocampus is uniquely important for episodic memory (memory for events that are specific to time and place) or whether the hippocampus is also important for learning and remembering facts (semantic memory). In two studies, we assessed the capacity for semantic memory in patients with bilateral damage thought to be restricted primarily to the hippocampal region who developed memory impairment at a known time. Since the onset of their memory impairment, the patients have acquired less factual knowledge than controls. The patients also exhibit temporally limited retrograde amnesia for factual information from the several years preceding the onset of memory impairment. Remote memory for factual knowledge (from 11-30 years before amnesia) is intact. The results show that the hippocampal region supports semantic memory as well as episodic memory and that its role in the acquisition and storage of semantic knowledge is time limited.

Retrograde and anterograde object-recognition memory was assessed in rats with cytotoxic lesions of the hippocampal formation (HPC), using a paradigm based on the natural tendency of rats to spend more time exploring novel objects than familiar objects. The rats were allowed to explore a sample object for 5 min/day on 5 consecutive days, either 5 weeks or 1 week before surgery. After surgery, retrograde recognition was assessed by comparing the amount of time spent exploring the sample versus a novel object in a free-choice situation. Control rats spent more time exploring the novel object than the sample objects from both presurgery time periods, whereas rats with HPC lesions did not discriminate between the novel objects and sample objects from either presurgery time period. Despite their deficits on the retrograde recognition test, the rats with HPC lesions performed like control rats on anterograde recognition tests, displaying a strong exploratory preference for novel objects over sample objects, with retention delays of either 15 min or 24 h. The findings suggest that extrahippocampal circuitry is capable of supporting object recognition, but only if the HPC does not participate in encoding the original encounter with the object.

We examined the performance of Long-Evans rats with 192 IgG-saporin lesions of the medial septum/vertical limb of the diagonal band (MS/VDB) or nucleus basalis magnocellularis/substantia innominata (NBM/SI), which removed cholinergic projections mainly to hippocampus or neocortex, respectively. We studied the effects of these lesions on anterograde and retrograde memory for a natural form of hippocampal-dependent associative memory, the social transmission of food preference. In a study of anterograde memory, MS/VDB lesions did not affect the immediate, 24-h or 3-week retention of the task. In contrast, NBM/SI lesions severely impaired immediate and 24-h retention. In a study of retrograde memory in which rats acquired the food preference 5 days or 1 day before surgery and they were tested 10-11 days after surgery, MS/VDB-lesioned rats showed striking memory deficits for the preference acquired at a long delay (5 days) before surgery, although all lesioned rats exhibited poorer retention on both retest sessions than on their pretest performance. Subsequent testing of new anterograde learning in these rats revealed no disrupting effects of lesions on a standard two-choice test. When rats were administered a three-choice test, in which the target food was presented along with two more options, NBM/SI-lesioned rats were somewhat impaired on a 24-h retention test. These results provide evidence that NBM/SI and MS/VDB cholinergic neurons are differentially involved in a social memory task that uses olfactory cues, suggesting a role for these neurons in acquisition and consolidation/retrieval of nonspatial declarative memory.

We studied the importance of the hippocampus and subiculum for anterograde and retrograde memory in the rat using social transmission of food preference, a nonspatial memory task. Experiment 1 asked how long an acquired food preference could be remembered. In experiment 2, we determined the anterograde amnesic effects of large lesions of the hippocampus that included the subiculum. In experiment 3, large lesions of the hippocampus that included the subiculum were made 1, 10, or 30 d after learning to determine the nature and extent of retrograde amnesia. Normal rats exhibited memory of the acquired food preference for at least 3 months after learning. Hippocampal lesions that included the subiculum produced marked anterograde amnesia and a 1-30 d temporally graded retrograde amnesia. The results show the importance of the hippocampus and related structures for nonspatial memory and also demonstrate the temporary role of these structures in long-term memory.

Focal retrograde amnesia is an unusual and theoretically challenging form of memory disorder. The case of a 65-year-old woman presenting with focal retrograde amnesia is reported. Following a cardiac arrest and subsequent hypoxia she remained in a coma for 24 h with evidence of epileptiform activity during the early recovery period. MR scans, 4 and 7 months post-onset, showed mild bifrontal atrophic changes mainly affecting white matter areas. An [18F]fluorodeoxyglucose resting PET scan 1-year post-onset demonstrated right occipito-temporo-parietal hypometabolism. We were able to document the patient's performance on an extensive range of anterograde and retrograde tests and to monitor her recovery of function by assessing her performance at 4, 12 and 24 months post-onset. Spared anterograde memory was observed on a range of verbal and non-verbal tests, including matched tasks that compared pre-illness and post-illness onset recollections. In contrast, her performance on retrograde memory tests, using detailed autobiographical and public events verbal and photographic tasks, showed a temporally-graded retrograde amnesia, more particularly affecting memory for autobiographical episodes. Possible mechanisms underlying CH's focal retrograde amnesia are discussed in terms of Damasio's time-locked multiregional retroactivation model.

Objective: To determine whether damage to prefrontal cortex is associated with face memory impairment., Background: Neurophysiologic and functional imaging studies suggest that prefrontal cortex is a key component of a distributed neural network that mediates face recognition memory. However, there have been few attempts to examine the impact of frontal lobe damage on face memory performance., Methods: Patients with focal frontal lobe lesions and normal control subjects were administered two-alternative forced-choice and single-probe "yes/no" tests of recognition memory for novel faces. Retrograde memory was assessed by using famous faces as stimuli., Results: Compared with control subjects, patients with frontal lobe lesions showed evidence of marked anterograde and relatively mild retrograde face memory impairment. In addition, patients with right frontal lesions demonstrated increased susceptibility to false recognition, consistent with the breakdown of strategic memory retrieval, monitoring, and decision functions., Conclusions: Prefrontal cortex plays an important role in the executive control of face memory encoding and retrieval. Left and right prefrontal regions seem to make different contributions to recognition memory performance.

A test of socially acquired food preferences was used to study the effects of large lesions to the hippocampal formation (HPC) on anterograde and retrograde memory in rats. In the anterograde test, rats with HPC lesions normally acquired the food preference but showed a faster rate of forgetting than control groups. When the food preference was acquired preoperatively, HPC groups exhibited a temporally graded retrograde amnesia in which memory was impaired when the preference was acquired within 2 days of surgery but not at longer delays. The results support the traditional theory that the HPC contributes to the consolidation of newly acquired information into a durable memory trace that is represented in other brain areas. Consistent with this view, the results indicate that, once a memory trace is consolidated, the HPC does not participate in its storage or retrieval. The possibility is considered that extrahippocampal areas in the medial temporal lobe are needed to maintain a memory trace throughout its existence.

A socially acquired food-preference test was used to assess effects of lesions to the frontal cortex on anterograde and retrograde memory in rats. In Experiment 1, there was no effect of lesion when rats were administered a two-choice test in which the target food was to be selected in the presence of a single distractor. In Experiment 2, a three-choice memory test was administered in which the target food was presented along with two equally palatable alternatives. In the latter test, lesioned groups displayed anterograde amnesia that increased with the length of the interval between postoperative acquisition and test, and a severe retrograde amnesia that extended equally over the entire range of intervals between preoperative acquisition and test. This outcome, which contrasted with the pattern of memory loss previously observed in rats with hippocampal lesions on this test, was interpreted as evidence for the strategic role of the frontal lobes in directing response selection and retrieval processes in memory.