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Dissociative amnesias have been reported in neurological episodes mild enough to not cause any visible lesions on morphological examination. Disproportionate retrograde amnesia with or without identity loss happens in the context of psychological trauma (known or not). In metabolic imaging studies, some authors have reported functional alterations, particularly in the bilateral hippocampus, right temporal regions and inferolateral prefrontal cortex, despite normal morphological imaging. To avoid the presumption of an organic, psychogenic or mixed origin for such changes, De Renzi et al. suggested the term 'functional amnesia' to describe the condition. Patients have sometimes recovered during events similar to those preceding the amnesia in either a spectacular fashion or never. Also, in some cases, distraction or sedation may trigger the start of recovery. During psychotherapy, one patient remembered seeing a car on fire when he was a boy, and his amnesia started when his house was on fire. This suggests control by the frontal cortex, with repression blocking amnesic traces in the new emotional and biological context., (Copyright © 2017. Published by Elsevier Masson SAS.)

Purpose of Review: Long-term memory impairments have great medical significance and a considerable health and economic burden. Understanding their cognitive and neuroanatomical underpinnings is of crucial importance. Severe amnesia is usually observed following bilateral hippocampal pathology. This review addresses the precise role of the hippocampus and related medial temporal lobe structures in amnesia., Recent Findings: Disagreements exist over whether, following selective hippocampal damage: retrograde amnesia for episodic memories is temporally limited or extensive and ungraded; anterograde amnesia involves both recollective and familiarity processes. It is accepted that material specific impairments follow unilateral medial temporal lobe damage, with verbal and nonverbal memory lateralized to left or right, respectively. Memory for unknown faces, however, may not depend on the hippocampus. Pharmacological studies in animals, with some extension to humans, highlight promising future therapeutic interventions targeting synaptic plasticity modulation., Summary: Despite considerable progress, some issues remain unresolved. The available evidence favours the view, however, that the hippocampus, in conjunction with other cortical areas, is critical for the retrieval of remote episodic memories and for both recollection and familiarity anterograde memory processes. There are as yet no effective pharmacological treatments for medial temporal lobe amnesia, but various rehabilitative techniques may be useful.

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.

This article reviews 147 cases of amnesia following damage including the hippocampus or fornix as reported in 179 publications. The aetiology, mnestic abilities and reference(s) are tabulated for each case. Consistent findings across cases include the association of bilateral hippocampal damage with a deficit in anterograde episodic memory combined with spared procedural and working memory. The limited nature of retrograde amnesia following lesions to the fornix is also noted. Less consistent and thus more controversial findings, include effects of lesion size or laterality, deficits in semantic memory or familiarity-based recognition and the extent of retrograde amnesia. The evidence concerning these issues is reviewed across cases.

In this paper, we describe some features of remote memory in a single-case, Y.K., with amnesic syndrome. His ability to access remote memory was investigated through a variety of tests and then analyzed in terms of specific aspects of remote memory, i.e., public events, personal semantic memory, and specific personal episodes. Although Y.K. showed relatively good performance in recalling public events, personal semantic memory, and general personal events, he was not able to recall specific personal episodes over his entire life span. That is, there appears a clear dissociation between recalling specific personal episodes and other aspects of remote memory. This suggests he lacks "richness" in his remote memory, which is probably necessary to maintain one's own identity.

An extensive battery of tests of anterograde amnesia and remote memory was given to ten amnesics with lesions either to the medial temporal lobes of the diencephalon. These showed that the patients had anterograde amnesia with deficits in verbal and non-verbal recall and recognition, but preservation of word stem completion and intelligence. Mild impairments on executive tests and digit span performance were largely caused by the poor performance of the Korsakoff patients. The amnesics also showed remote memory deficits for personal and public domain information, and temporal gradients were observed for some of the tests. These deficits probably arose because the patients' anterograde amnesia was more severe than their retrograde amnesia even for the recent pre-morbid past. They were more impaired in the recall of details about famous names in their ability to recognize such names. There was also a suggestion that performance on anterograde tests did not relate strongly to that on tests of retrograde amnesia of the remote pre-morbid past. However, this effect was less apparent with memory for personal information when the format and the information tapped were matched on pre- and post-morbid tests.

This article reviews recent studies of memory systems in humans and nonhuman primates. Three major conclusions from recent work are that (i) the capacity for nondeclarative (nonconscious) learning can now be studied in a broad array of tasks that assess classification learning, perceptuomotor skill learning, artificial grammar learning, and prototype abstraction; (ii) cortical areas adjacent to the hippocampal formation, including entorhinal, perirhinal, and parahippocampal cortices, are an essential part of the medial temporal lobe memory system that supports declarative (conscious) memory; and (iii) in humans, bilateral damage limited to the hippocampal formation is nevertheless sufficient to produce severe anterograde amnesia and temporally graded retrograde amnesia covering as much as 25 years.

We recorded auditory event-related potential (ERP) by using the standard oddball paradigm in seven amnestic patients. Patients were divided into three groups according to brain CT or MRI findings. (1) Three patients with no detectable lesion, including two patients studied during the episode of transient global amnesia, showed a well-defined P300. (2) Three patients with detectable lesions in the mesial temporal lobes did not show any wave form corresponding to P300. In two of these three patients, the ERP wave form showed a significant change in accordance with the improvement of MRI findings. (3) One patient who had a hypothalamic lesion due to total resection of craniopharyngioma showed a low-amplitude P300. Although neuropsychological examinations showed selective and severe impairment of recent memory function in all of these patients, no significant relationship was found between the degree of memory disturbance and P300 abnormality. These results suggest that P300 is more affected by existence and extension of brain lesions, especially in the mesial temporal lobes, rather than degree of memory disturbance. However, these results do not necessarily suggest that the potential generated in the mesial temporal lobes is directly recorded as a component of the scalp-recorded P300.

We report the first human case of combined mammillary body and medial thalamic lesions due to focal pathology. A patient presented with a multi-lobular lesion that affected the mammillary bodies, the medial thalamus and the brain stem. On neuropsychological testing, he showed significant anterograde memory impairment, with marked impairment on delayed story recall, but normal or only mildly impaired performance on retrograde memory tasks. Our findings corroborate the results of recent non-human lesion studies and indicate that some of the well-established features of the amnesic syndrome, such as severe retrograde amnesia, may not be due to primary diencephalic pathology. Significant retrograde amnesia may result from cortical pathology or from an interaction between cortical and subcortical pathology.

The purpose of the present study was to examine explicit and implicit memory for auditory events presented immediately prior to sleep onset. The results of the present study suggest subjects allowed 10 minutes of sleep demonstrate deficient explicit memory for auditory stimuli presented immediately prior to sleep onset. Subjects showed severe free recall deficits for word pairs presented 3 minutes prior to sleep onset and recognition deficits for stimuli from 1 minute prior to sleep onset. Implicit memory for word pairs presented prior to sleep onset seemed intact, and no recency effect was observed. In contrast to the 10-minute condition, subjects allowed 30 seconds of sleep demonstrated no equivalent explicit memory deficits. Memory performance in both delay conditions, however, appeared globally impaired relative to control data from subjects who remained awake. The results are interpreted in terms of elaboration of stimulus encoding, interruption of consolidation and retrograde versus anterograde amnesia.

This study examined the memory performance of patient RK who developed substantial memory impairments due to a hypothalamic glioma but in the absence of any evidence of frontal disturbance. RK was evaluated on both tests of anterograde and retrograde memory for temporal context. In the first experiment he exhibited marked deficits on a list discrimination task even when recognition performance was well within control range. Experiment 2 confirmed this disproportionate impairment of temporal order memory and showed that RK's list discrimination deficit was as severe as that found in alcoholic Wernicke-Korsakoff Syndrome patients. Experiment 3 showed that RK's temporal discrimination deficit was not a general deficit in discrimination because he performed normally on a spatial discrimination test of comparable difficulty to the temporal task. Experiment 4 examined RK's memory for deceased famous people and his ability to indicate the half decade in which they died. RK's performance was indistinguishable from controls whereas WKS patients were extremely impaired. This study adds to the view that frontal damage is not a necessary condition for impairment on anterograde measures of temporal context memory. However, further evidence from this study indicates that temporal judgments about pre-existing memories may depend on intact frontal lobe functioning.

A patient with an extremely long-standing low grade glioma affecting the left temporal lobe is described. The patient was almost entirely unable to retrieve the names of current personalities, although in other respects identification was unimpaired and nominal functions were only mildly inefficient. In particular geographical features and historical figures were generally appropriately named. The problem was equally severe whether naming was to confrontation, from description or by generation. A similarly severe impairment was also found for the retrieval of new words that had come into the language in the last twenty years (eg. aids). The impairment of retrieving people's names was interpreted in terms of a long-standing inability to form new associations between meaning and phonological word-forms.

The sudden resurgence of precise information some time after the failure of its recall (memory block) suggests the intervention of unconscious processes. In normal subjects the experimental demonstration of such processes meets with methodological snags. They are avoided in patients with a pure amnesic syndrome because retrograde amnesia produces many instances of missing memories, while anterograde amnesia prevents the patient from consciously thinking about it. Three patients with a pure amnesic syndrome were submitted to 4 interviews over 12 days on 3 topics concerning places and itineraries that were very familiar before the disease, and a shocking event of their life. Retrieved memories were compared to those of normal matched subjects. The results showed a dramatic increase for memories of places and itineraries over sessions, and the absence of improvement of autobiographical memories. These findings underline the role of the activation of unconscious processes in recall and the different status of semantic and episodic memory.

Establishing the precise relationship between anterograde amnesia (AA) and retrograde amnesia (RA) has implications for psychological and neuroanatomical models of memory. Many patients have been described who demonstrate AA in conjunction with RA or who demonstrate AA with little, or no apparent, RA. Intact anterograde memory in conjunction with deficits on tasks of retrograde memory is rarely encountered. In this paper, we describe a young female patient (LD) whose RA is extremely severe when contrasted with her mild to moderate deficits on tasks of verbal anterograde memory. In addition, on tests of episodic and semantic autobiographical memory, LD appeared more impaired in her recall of specific episodes than of factual information about her past. The importance of this dissociation in RA for the episodic-semantic distinction and the possible role of visual imagery in recalling remote episodic events are discussed.

Two patients developed anterograde amnesia following the apparently uncomplicated transcallosal-transventricular removal of a colloid cyst. Damage to the fornical columns was demonstrated on CT and MRI scans, whilst other memory related structures were entirely normal. Longitudinal neuropsychological evaluation, over 12-24 months, has revealed a very similar pattern of deficit in the two cases: verbal memory has remained persistently impaired whilst nonverbal anterograde memory has improved to some degree. Formal tests of remote public (famous faces and events) and personal autobiographical memory have supported the clinical impression that neither patient has a temporally extensive retrograde amnesia. These findings address the role of the fornix, and the dissociation of memory processes in humans.

We report a patient who was evaluated neuropsychologically and with single photon emission computed tomography (SPECT) during and after an episode of transient global amnesia. During the attack, there was patchy retrograde amnesia and an inability to learn both verbal and non-verbal material. SPECT showed severe bitemporal hypoperfusion. Serial neuro-psychological testing documented a rapid recovery of recognition, but delayed recovery in reproduction of learned information. Recovery of spontaneous verbal and figural fluency was even further delayed. Follow up SPECT examination showed a recovered cerebral perfusion. This case supports the hypothesis that TGA is associated with transient hypoperfusion of bilateral medial-temporal brain structures and suggests an additional involvement of structures responsible for drive and initiation.

Remote memory performance was assessed in a carefully matched sample of temporal lobectomy subjects and normal controls. Left temporal lobectomy subjects exhibited a consistent pattern of remote memory disturbance. Right temporal lobectomy subjects performed at the same level as normal controls. The pattern of impairment observed in left temporal lobectomy subjects was characterized by deficits in recall of chronological information from the past decade and extended to deficits in recall in some aspects of factual knowledge. The disorder could not be attributed solely to language deficits and was at least as severe as accompanying deficits in recent memory. These findings suggest that the left medial temporal region may play a significant role in recall of remote information in addition to its role in recent memory functions.

A variety of manipulations which interfere with the activity of the striatum, including cholinergic blockade and spreading depression, produce amnesia. However, it has been demonstrated that with overtraining, striatal spreading depression and injections of anticholinergic drugs do not produce memory deficits in positively-rewarded tasks. In the present experiment 2% lidocaine was injected into the striatum shortly after training of passive avoidance, using three levels of footshock (0.2, 0.3, and 0.4 mA). Highly significant retention deficits were produced when the lower intensities were studied; in contrast, the animals trained with 0.4 mA showed near-perfect performance. The data show that the enhanced learning experience, which may be equivalent to overtraining, also protects against memory deficits in negatively-rewarded behaviors, and suggest that it induces a transfer of mnemonic functions from the striatum to other neural structures.

The paper deals with analysis of the influence of blockade of separate components of benzodiazepine-GABA-ionophore complex on the recovery of memory trace amnesia under GABA-A and GABA-B receptors activation in the experiments with conditioned reaction of passive avoidance of mice. Activation of GABA-A receptors did not change the behavioural amnesia manifestation at all terms of testing. Activation of GABA-B receptors before learning and amnestic influence caused spontaneous recovery of avoidance reaction. Blockade of chloride channel by picrotoxin and of benzodiazepine receptor by flumazepil restored the reproduction of the memory trace disturbed against the background of GABA-B receptors activation. Systemic flumazepil administration contributed to the memory trace reproduction against the background of GABA-A receptors activation by muscimol in the dose of 0.5 mg/kg. In conditions of amnesia development against the background of muscimol in the dose of 1 mg/kg the blockade of any component of benzodiazepine-GABA-ionophore complex was not effective. The obtained data testify that activation of GABA-A and GABA-B receptors changes the amnesia development and correction of amnesia memory trace by the blockade of separate components of benzodiazepine-GABA-ionophore complex.

Retrograde amnesia (RA) was studied in patients with Huntington's disease (HD) or Alzheimer's disease (AD) using an updated version of the remote memory battery originally developed by Albert, Butters and Levin. Regardless of whether remote memory was measured by unaided recall or cued recall, HD patients exhibited deficits that were equally severe across decades. RA was more severe in AD than in HD patients and the AD patients recalled significantly more items from the 1940s and 50s than from the 60s, 70s or 80s. The AD patients also displayed dysnomia, while the HD patients did not. Naming difficulties appeared to contribute to the poor overall performance of the AD patients, but did not account for the temporal gradient of their RA. These findings, like recent reports focusing on these patients' ability to learn new information and to search semantic memory, indicate that the processes underlying AD and HD patients' memory failures are distinct.

This single case study describes our investigations of the retrograde memory deficit of a patient who became severely and selectively amnesic after an encephalitic illness. On clinical assessment his retrograde deficit for both personal and public events appeared to encompass his entire adult life. However, he retained knowledge of words introduced into the vocabulary during the retrograde period. The experimental investigation documented his inability to recall, recognize, and place in temporal order the names and faces of famous people for all time periods sampled. By contrast, his recall of either a famous face or a famous name was significantly facilitated by the verbal cue of the person's first name and initial of the surname (i.e., Margaret T...). His performance on a test of "familiarity" that required him to select the famous name or the famous face from two distractors (unknown) was within normal limits. It is argued that names and faces of famous people are represented in more than one system: both in a vocabulary-like fact memory system that is preserved and also in a congnitively mediated schemata that in this case is functionally inoperative.

The effect of hippocampal denervation on olfactory memory in rats was tested after interrupting the lateral olfactory tract projections at the level of the entorhinal cortex. When lesioned animals were trained to learn new odors, they showed no evidence of retention 3 h after acquisition. These results confirm earlier data on rapid forgetting in rats after hippocampal deafferentation and are in parallel to the anterograde amnesia typically found in humans with hippocampal damage. On the other hand, preoperatively learned information was minimally impaired after hippocampal deafferentation even if it was acquired within less than 1 h before the lesion. This finding differs from reports on humans as well as monkeys with hippocampal damage where memories formed during a critical time span of months or even years before the lesion are found to be impaired. This may suggest that the consolidation process in humans and rodents has different time scales or that the roles of the human and the rat hippocampal structure in memory formation are somewhat different.

Two experiments examined the extent to which retrograde amnesia (RA) is attenuated by prior learning experiences. In Experiment 1, rats initially received either passive avoidance training in a step-through apparatus, exposure to the apparatus, or noncontingent footshock. When training on a second but different passive avoidance task was followed by hypothermia treatment, RA was obtained only in the latter two groups. In Experiment 2, one-way active avoidance training, yoked noncontingent shocks, or apparatus exposure constituted the initial experience. Subsequent step-down passive avoidance training and amnestic treatment resulted in memory loss for the prior apparatus exposure group, but not for either of the preshocked conditions. These experiments demonstrate that certain types of prior aversive experience can substantially modify the magnitude of RA, and, in conjunction with other familiarization studies, emphasize a paradox for interpretations of RA based solely upon CNS disruption. The possibility that hypothermia treatment serves as an important contextual or encoding cue necessary for memory retrieval was considered. It was suggested that prior experience may block RA by enabling rats to differentiate training and treatment conditions.

Mice were given a single training trial and then received either sham treatment or electroconvulsive shock (ECS; four treatments at hourly intervals) at 1 of 7 times (1-70 days) after training. Retention was always tested 2 weeks after treatment. Control animals exhibited gradual forgetting with increasing retention intervals. Mice given ECS exhibited severe retrograde amnesia, which diminished as the interval between training and ECS increased from 1 to 21 days. ECS given 21-70 days after training had no effect on memory. The finding of long, temporally graded retrograde amnesia in mice establishes continuity between the results for laboratory animals and those for humans and indicates that the neural changes involved in the consolidation of memory can continue for a significant portion of the lifetime of a memory.

Lysine vasopressin (1 microgram/rat SC) administered 1 hr prior to either the acquisition trial or 24 hr retention trial facilitated passive avoidance retention. Amnesia was produced when a single 50 mg/kg (IP) injection of pentylenetetrazol was given immediately following the passive avoidance acquisition trial. A single injection of lysine vasopressin (1 microgram/rat SC) administered 1 hr prior to either the acquisition trial or 24 hr retention trial antagonized the amnesia.

Rats were used to examine the effects, upon a conditioned aversion to cold drinking water, of electroconvulsive shock (ECS) delivered during the delay between cue and unconditioned stimulus. An injection of LiCl (US) 30 min after ingestion of novel cold water (CS) produced a reliable aversion to the cold water. ECS given immediately following the ingestion of cold water substantially attenuated this aversion. An orderly decrease in the attenuation of the aversion was observed when ECS was delayed 5, 10 or 20 min after offset of the cold water cue. The results indicate that ingestive cue aversions can be formed without electrochemical neural-transmission-based representation of the cue being maintained during the CS-US interval. The differential effectiveness of ECS suggests that this agent retroactively interferes with processing of the ingestive cue.

Subseizure electrical stimulation of the amygdala produced retrograde amnesia for a visual discrimination shock-motivated task. Animals pretreated with the alpha-adrenergic antagonist phenoxybenzamine, or the beta-adrenergic antagonist propranolol, did not develop amnesia. The findings indicate that adrenergic antagonists attenuate amnesia produced by amygdala stimulation for visual discrimination training. These results are consistent with previous evidence indicating that adrenergic antagonists attenuate the amnesias produced by a variety of agents, and thus, suggest that adrenergic mechanisms may be involved in the production of retrograde amnesia.

The author, by giving an outline of one particular case as well as a survey of the relevant literature on transient global amnesia, describes the characteristic clinical picture that is characterized by a sudden loss of what is known as the short-time memory, which usually lasts for several hours, as well as by retrograde amnesia which sometimes dates back to many years. The condition gradually fades away within a few hours or during a night's sleep, and what remains is lack or loss of memory for the episodic period or sometimes retrograde amnesia. Relapses were not observed in the majority of patients. The disease usually develops in people in their sixth to eighth decades of life. The cause of the disease is not yet fully understood. Accordingly, it is justified to use such terms as autochthonous or cryptogenic amnestic episodes. The disease is also discussed from a differential diagnosis point of view.

Disrupting circadian organization by exposing rats to a shifted illumination schedule after training for passive avoidance and shuttle box avoidance behavior resulted in retrograde amnesia as evidenced by impaired performance during retention and extinction testing respectively. A single treatment with either the ACTH-(4-9) analog ORG 2766 or desglycinamide9-(Arg8)-vasopressin (DGAVP) 1 hour prior to the retention of passive avoidance or extinction of shuttle box avoidance behavior restored the behavioral impairment. It is suggested that these peptides may be useful to relieve memory deficits induced by disturbances in circadian organization.

Restoration of memory by pretest reminder treatments following ECS-induced amnesia in principle could be mediated by nonassociative arousal and/or reactivation of information by the reminder stimuli. In the present research, arousal value of the reminder treatment was largely a function of the novelty of the context in which the reminder cues occurred. After producing ECS-induced amnesia in rats for a signaled passive avoidance task, presentation of the signal outside of the training and test context proved to be an effective reminder cue. However, prereminder familiarization with the reminder location, which was sufficient to reduce exploratory behavior suggestive of a decrease in the arousal value of the context, did not influence recovery from amnesia. These data indicate that reminder treatments are capable of reversing experimental amnesia by initiating further processing of previously acquired information even when the treatment does not produce appreciable arousal.

The time course of antirecall effect and grades of sedation after the oral administration of diazepam and lorazepam were determined in 120 patients. Three standard doses of each drug were employed. Grades of sedation following oral diazepam were dose related, with a latency of 30-60 min and duration of 120-150 min. All three doses of lorazepam produced significantly more sedation with a similar latency (30-60 min) but longer duration (more than 240 min). Peak frequencies of the antirecall effects of diazepam 10, 15, and 20 mg were 5, 20, and 30 per cent, respectively. The duration was about two hours. Peak frequencies of the antirecall effect after lorazepam 2, 3, and 4 mg were 30, 45, and 72 per cent, respectively. Latency of peak action was about 60-90 min for all the doses, but the duration, especially with 3 and 4 mg doses, was long (4 h).

Aging mice showed a retrograde amnesia for passive avoidance behavior when a single electroconvulsive shock (ECS) was given at post-training intervals up to 1 h, whereas adult mice showed no significant amnesia when ECS was given 10 min or more after training. Catecholamines (norepinephrine and dopamine), but not serotonin (5-HT) changed with aging in the several brain regions, but only 5-HT was significantly changed (elevated) by ECS. Protein synthesis was significantly inhibited by ECS, notably in limbic structures. The increased susceptibility of aging mice to the amnesic effect of ECS could be related to aging-related changes in the rate of memory consolidation or to the duration of neural chemical changes that disrupt processes such as consolidation, storage, and/or retrieval of the memory trace.

Formal neuropsychological evaluation in patient with transient global amnesia (TGA) associated with migraine was performed 6 days and 17 months after the episode. Verbal learning difficulties and verbal IQ deficit were observed in line with the neuropsychological profile seen in the follow-up of TGA. A common origin for the TGA-Migraine episode and isolated TGA is discussed.

Rats were conditioned to fear a tone paired with shock to the feet. Retention tests 4 days later showed that consolidation had occurred. Other animals were not tested for retention at 4 days, but the tone was presented in order to reactivate their memories of the conditioning. An amnesia gradient was generated by low-intensity electrical stimulation of the amygdaloid complex at different intervals after the tone, but stimulation was without effect either when given to rats not previously conditioned or when given to conditioned rats without preceding memory reactivation. Thus, stimulation of the amygdaloid complex can can affect memory retrieval. Moreover, the data call into question the assumption that an amnesia gradient indicates that the memory consolidation process has been modified.

In the present study the effects of intracerebroventricularly [icv] administered somatostatin [linear and cyclic], somatostatin3-6, somatostatin7-10 and des AA1,2,4,5,12,13 [D-Trp8] somatostatin [ODT8-SS] were investigated on electroconvulsive shock [ECS]-induced retrograde amnesia in rats. The ECS significantly decreased the foot shock-induced avoidance latency, and thus caused retrograde amnesia. Somatostatin [linear and cyclic] in a dose of 0.6 nM had no action on the ECS-induced retrograde amnesia, while in doses of 3 nM and [cyclic only] 6 nM it significantly prevented it. Somatostatin3-6, somatostatin7-10 and ODT8-SS in doses of 0.6, 3 and 6 nM had no effect on the ECS-induced amnesia. These results indicate that the whole sequence of the original somatostatin molecule is needed to block the ECS-caused retrograde amnesia.

Naive and pretrained rats were trained in two active avoidance paradigms using a pole-climbing box and in a single-trial passive avoidance task using a T-maze. They were then subjected to amnestic treatments with electroshock, leptazol, pentobarbitone, or ether anesthesia. Single retention tests were given at 20-24, 44-48, or 68-96 h posttreatment. Electroshock and leptazol seizures produced retrograde amnesia in all three paradigms, provided that seizures were maximal and retention was tested before 48 h. Prior treatment with anticonvulsant drugs prevented amnesia. Ether and pentobarbitone anesthesia failed to produce amnesia in all three tasks. A trend of recovery from amnesia was observed in the electroshock and leptazol groups when tested for retention 48-96 h posttreatment. On the other hand, the non-amnesic control, pentobarbitone, and ether groups showed signs of forgetting at these longer intervals. Consolidation failure and/or retrieval block was surmised to be the cause of amnesia; recovery was the possible result of removing the block.

In this study, the possible role of overt convulsions following pentylenetetrazol (PTZ) in retrograde amnesia was investigated. Following a single passive avoidance conditioning, when overt convulsions were blocked with sodium pentobarbital (Nem), the amnesic effect of pentylenetetrazol was also blocked. Subconvulsive doses of the drug did not produce amnesia. Animals that received a typically convulsive dose of the drug but failed to convulse were not amnesic; only animals with overt convulsions were different from saline controls. The data suggest that overt convulsions may be necessary for the development of pentylenetetrazol-induced retrograde amnesia.

The effects of several doses of intracerebroventricularly injected cholecystokinin octapeptide sulfate ester (CCK-8-SE) and nonsulfated scholecystokinin octapeptide (CCK-8-NS) were studied on electroconvulsive shock (ECS)-induced retrograde amnesia, as measured in a one-trial step-through passive avoidance paradigm. Both CCK-8-SE and CCK-8-NS were able to attenuate amnesia slightly when they were injected into rats 10 min prior to ECS treatment, possibly by reducing the severity of the ECS-induced seizures. Of the treatments carried out immediately after ECS, only the 0.8 pmole dose of CCK-8-NS could significantly restore retrograde amnesia. After treatment 20 min prior to testing 24-hr retention, no effect of the peptides was observed. The lack of a dose-dependency and of any effect on retrieval raises the possibility that the CCK octapeptides influence memory processes by an indirect mechanism.

Post-trial injections of norepinephrine (NE) or cycloheximide (CHX) into the amygdala produces a long-term retention deficity (amnesia) for a 1-trial footshock experience in rats. concomitant post-trial injections of the adrenergic antagonist, propranolol, prevents NE-, but not CHX-induced amnesia. These results indicate separate mechanisms of action for amnesia produced by intracranial CHX and NE injections.

Although there have been several reports that preweanling rats and mice are relatively resistant to experimentally induced retrograde amnesia, there is virtually no information concerning susceptibility to anterograde amnesia in subjects of this age. Therefore, in the present experiment, 23-day-old rats received hypothermia either prior to, or immediately after, punishment training in an attempt to induce anterograde and retrograde amnesia, respectively. When tested 24 hr later, only those subjects given hypothermia prior to training exhibited any loss of retention. Thus these results confirmed previous evidence of resistance to retrograde amnesia in preweanling rats and further demonstrated that substantial anterograde amnesia could be obtained in these subjects. Performance of subjects tested after a 5-min retention interval revealed that the poor retention performance in subjects cooled prior to training and tested 24 hr later was not due to a learning deficit. These results are also discussed with respect to the issue of the independence of anterograde and retrograde amnesia.

To analyze disorders of memory functions, observations were made in healthy test subjects after administration of psychotropic drugs and anesthetics. In isolated cases amnesic episodes were recorded and in 8 of the subjects accurate measurements of the retrograde amnesia after propanidid anesthesia were made. The observations provided arguments for the delimitation of the immediate memory (ultra-short-term memory, one minute memory) from short-term memory and long-term memory of the conventional terminology. As a result of our investigations we came to the thesis that the transformation of the non-specific biochemical and electrophysiological processes underlying the immediate memory into the specific processes underlying the short-term memory is more susceptible to disturbances than that of reproduction and the processes serving for perception. With regard to forensic assessment, it is significant that behaviour foreign to the personality could not be observed in amnesic episodes.