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PubMed1982

Delayed post hypoxic transient amnesia is not associated with electrical brain seizures.

Rats rendered hypoxic by brief exposure to N2 after learning an avoidance response go into convulsions and subsequently become amnestic. Overt convulsions can be avoided whilst yet producing delayed post-hypoxic transient amnesia (DPHTA) by using 2% O2 in N2 in place of pure N2. The experiments reported here show that with this gas mixture, the ECoG shows hardly any of the electrical activity associated with seizures which occurs with N2. It is concluded that electrical seizures are not associated with the mechanism responsible for DPHTA.

Animals↗
PubMed1981

Time dependent changes in anterograde scopolamine-induced amnesia in rats.

These experiments studied the effect of scopolamine on memory formation and subsequent memory recall. Different groups of rats were trained on a Y-maze brightness discrimination task 20 min after IP injection of 2 mg/kg scopolamine HBr, an anticholinergic. Retention tests were then conducted 1 day or 2, 4, or 6 weeks after training. Deficits in retention performance were observed at 1 day and 2 weeks after training but not at the longer intervals. In addition, other rats were trained in the same manner and after the same dose of scopolamine but were then retention tested 20 min after 0.5 mg/kg physostigmine salicylate, a cholinesterase inhibitor. These subjects also showed deficits at 1 day and 2 weeks but were not different from controls at the longer intervals. Amnesia was not, however, produced after treatment with scopolamine methyl nitrate or by injections of scopolamine HBr administered immediately after training. These results suggest that scopolamine, present in the central nervous system during training or within the first few moments thereafter, modifies the formation of the memory trace in such a way that memory is not available for recall for a period of weeks.

Animals↗
PubMed1982

Alleviation of anisomycin-induced amnesia by pre-test treatment with lysine- vasopressin.

Amnesia in mice for a passive avoidance response induced by anisomycin injection immediately after training was reversed by 40 micrograms of lysine-vasopressin given one hour before testing. Control groups receiving non-contingent shock instead of training were used to demonstrate that the effects of vasopressin were due to memory of shock received in a particular place, rather than non-specific suppression of locomotion. The effects of vasopressin on retention were not mimicked by either pentylenetetrazol or epinephrine suggesting that the enhanced latencies were probably not the result of increases in fear or arousal. These data support the hypothesis that the retrieval of memory can be facilitated by vasopressin. The possibility of a relationship between the effects of vasopressin and those of catecholamine manipulations on memory is discussed.

Animals↗
PubMed1992

Learning of rats under amnesia caused by pentobarbital.

Dissociated learning of rats in the normal state and the state of amnesia produced by pentobarbital (15 mg/kg, ip) was carried out. Rats were trained to approach a shelf where they received food reinforcement. In Group 1 the rats were trained under the influence of pentobarbital to run to the same shelf as in the normal state. In Group 2 the rats were trained to approach different shelves in different drug states. It was shown that memory dissociation occurred in both groups. Differences in the parameters of training under the influence of pentobarbital between Groups 1 and 2 were revealed. These findings show that the brain-dissociated state induced by pentobarbital is formed with the participation of the mechanisms of information perception.

Animals↗
PubMed1992

A threshold for the protective effect of over-reinforced passive avoidance against scopolamine-induced amnesia.

Acetylcholine-receptor blockers produce amnesia of aversively motivated behaviors. However, when animals are submitted to relatively high intensities of footshock (over-reinforcement), anticholinergic treatment does not induce memory impairments. The aim of this work was to determine whether the antiamnesic effect produced by increasing the magnitude of the negative reinforcer is gradually established or if a threshold should be reached to obtain such an effect. Wistar rats were trained in passive avoidance using 2.5, 2.6, 2.7, 2.8, 2.9 or 3.0 mA; 5 min after training they were given one systemic injection of scopolamine (8 mg/kg). An amnesic state was produced in the groups that were trained with the lower intensities (2.5-2.7 mA); with the three higher intensities near-perfect retention was evident. These results suggest that acetylcholine is critically involved in memory consolidation, and that by increasing the magnitude of the negative reinforcer, a threshold is reached where cholinergic activity of the nervous system is not necessary for the development of the consolidation process.

Animals↗
PubMedDate not supplied

Pramiracetam effects on scopolamine-induced amnesia in healthy volunteers.

Pramiracetam has been evaluated for its potential antiamnesic properties in scopolamine-induced amnesia in healthy volunteers. Two groups of twelve males, 18-42 and 55-65 years old, respectively, were randomly assigned to oral treatment with pramiracetam (600 mg twice a day) or with placebo for 10 consecutive days. On day 11 each subject was injected intramuscularly with scopolamine hydrobromide (0.5 mg). Before scopolamine injection and then 1, 3 and 6 h after it, subjects were administered the following psychometric tests: simple and choice visual reaction times, digit symbol substitution test, Rey's 15 words test for short and long term verbal memory. Scopolamine significantly impaired episodic memory and selective attention tests in both scopolamine and placebo groups. Instead visuo-motor and incidental learning measures were unaffected. Pramiracetam, when compared to placebo, was able to partially reduce the amnesic effects induced by scopolamine both in young and old subjects.

Clinical Trial↗
PubMed1993

Is aluminium an etiologic contributor to alcoholic amnesia and dementia?

Neurotoxicity from excess brain exposure to aluminium (Al) is well-documented, from both clinical observations and animal experiments, to impair learning, memory and cognition. The etiology of the cognitive impairment in chronic abusers of ethanol--alcoholic amnesia or dementia--is not known, but it is likely to be multifactorial. We hypothesize that a slowly-progressive accumulation of Al in the brain, so as to reach functionally-toxic levels, may be one such factor. This could occur because of an increased permeability of intestinal mucosa to entry of Al, arising from sustained exposure of the gastrointestinal tract to alcoholic beverages, plus a trend for more frequent ingestion of antacids based on Al salts for treating gastritis or ulcers caused by such exposure. If this be true, use of Al-containing medications, as well as all avoidable exposures to Al, should be contra-indicated for chronic heavy drinkers.

Alcohol Amnestic Disorder↗
PubMed2000

Memory for object locations in Korsakoff's amnesia.

Deficits in spatial context memory are an important characteristic of Korsakoff's amnesia. In memory for spatial context information, there is evidence for a functional dissociation of three separate processes: (1) binding of object information to locations (i.e. binding complex memories), (2) exact, metric processing of Euclidean co-ordinates, and (3) an integration mechanism. In the present study, these sub-mechanisms were assessed experimentally in a group of Korsakoff patients (N = 20) and compared to healthy controls (N = 20) to see whether selective deficits can be demonstrated. It was found that Korsakoff patients display deficits on all three spatial-memory conditions, which are not the primary result of deficits in visuo-spatial construction and memory for object identity. No evidence for selective impairments could be observed. These impairments can be linked to damage of diencephalic regions and perhaps the parietal cortex.

Female↗
PubMed1992

Memory for what it is and memory for what it means: a single case of Korsakoff's amnesia.

A single case of Korsakoff's syndrome, showing classic circumscribed amnesia on traditional neuropsychological tests, performed a number of learning tasks previously used in primates to demonstrate the different anatomical basis of memory systems used to learn about the properties of objects or to learn about rules of responding. The patient (CJ) performed in a manner very similar to lesioned monkeys in that he could learn evaluative tasks (e.g. a red object is nice), but not rule based tasks (e.g. a red object means go left). In consequence CJ learned an object discrimination task in a manner qualitatively different from a group of non-amnesic controls. Although he could not learn rule based tasks, CJ could perform them once he had been given the rule. Detailed analysis of learning showed that CJ could choose the object he had chosen previously, but could not say where it had been or whether he had been rewarded. Furthermore he could recognise a word as familiar, while not remembering its source. We propose that he has a specific impairment in a memory system concerned with the representation of the signification of objects in particular contexts, while representation of the properties of objects remains intact.

Alcohol Amnestic Disorder↗
PubMed1993

Spatial memory in amnesia: evidence from Korsakoff patients.

Two experiments are reported which investigated a hypothesised disproportionate deficit in amnesic spatial memory. Korsakoff amnesic memory for the locations of objects or words placed on a grid was compared to control memory which had been attenuated by longer delays before testing. The effects of incidental versus intentional encoding of the locations were compared. No significant evidence of a disproportionate spatial memory deficit in Korsakoff amnesia was found, intentional instructions did not improve Korsakoff amnesic spatial memory scores, and there was no significant evidence of a trade-off of item memory and location memory specific to the Korsakoff amnesic group. Rather, intentional instructions significantly reduced item memory in both Korsakoff amnesics and normal controls, while having no effect on spatial memory. When location was scored by lenient criteria, there was no significant difference between groups for this measure, nor for recall and recognition memory for these items. Thus Korsakoff amnesic memory was very similar to that of control memory attenuated by longer delays before testing. The Korsakoff amnesic subjects' memory therefore differed quantitatively rather than qualitatively from that of control subjects' memory.

Adult↗
PubMed1994

The failure of context shifts to alter the recognition of faces: implications for contextual deficits in amnesia.

The effects of contextual changes were examined in a group of divers performing a test of face recognition. No evidence was found that the shift from above to below water, or vice versa, disrupted recognition. The fact that the same test of visual recognition is sensitive to amnesic subjects poses a challenge to certain versions of the contextual deficit theory of amnesia.

Adult↗
PubMed1997

Effects of flunarizine and nitrendipine on electroconvulsive shock- and clonidine-induced amnesia.

This study was designed to examine the calcium channel blockers flunarizine and nitrendipine for their ability to prevent electroconvulsive shock (ECS)- or clonidine-induced deterioration of the inhibitory avoidance performance (step-down) in rats. Flunarizine (10 mg/kg) and nitrendipine (40 mg/kg) were found to prevent the ECS- or clonidine-provoked amnesia after oral administration for 12 days. The mechanisms of action of the two drugs are considered. The results of this study further suggest that calcium antagonists might be useful in the treatment of cognitive disorders.

Adrenergic alpha-Agonists↗
PubMed1983

Presentation of a flashing light following training produces amnesia.

Long-Evans rats given exposure to a flashing-light stimulus following one-trial fear conditioning showed amnesia relative to controls not given the flashing-light experience. Together with previous results obtained in this laboratory, it is apparent that the flashing light modulates memory processing.

Animals↗
PubMed2001

Memory disruption in rats with nigral lesions induced by MPTP: a model for early Parkinson's disease amnesia.

Intra-nigral administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyrindine (MPTP) caused a lesion in the substantia nigra, compact part (SNc) and a specific loss of dopamine and its metabolites in the striatum of rats. The animals were then tested in the two-way active avoidance task. MPTP-treated animals presented lower learning scores in the training and test sessions, an effect that was not caused by motor impairment or by a decreased sensitivity to footshock since their reaction time to the footshock (unconditioned stimulus - UCS) was not reduced. These lower scores were also not attributable to lower acoustic sensitivity or to a slowing in the association of the sound cue (conditioned stimulus - CS) with the UCS since the reaction time to the CS in the active avoidance response did not differ between MPTP-treated and control groups. Therefore, these results are more properly attributable to an impairment of the memory acquisition and retention processes. In addition, this study is presented as a model of early Parkinson's Disease amnesia and is discussed in terms of the importance of the nigrostriatal pathway to memory acquisition and storage processes.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1988

[Sleep and dreams in Korsakoff's amnesia due to alcoholism].

Sleep and dreams in 15 chronic alcoholic patients with amnesia were compared with sleep and dreams of 15 age- and sex-adjusted normal subjects. The patients were subjected to psychological tests in order to determine their I.Q. and their memory disturbances. All subjects had two nights of polygraphic recordings; the first tested the natural sleep organization. During the second night, they were awakened 7 min after the onset of each REM sleep episode, and, at least once, 20 min after the onset of a stage II episode, in order to record on a tape their dream reports according to a standardized protocol. The sleep patterns of the amnesic patients did not show any significant alteration. However, after wakening during the night, patients exhibited a higher tendency to return to REMS than controls. There was still some dream activity in those patients, although noticeably less frequently, and their dream activity had a very poor verbal expression. However, there was no change with respect to the spatio-temporal organization, sensorial perceptions, motor activity and verbalizations during their dreams.

Adult↗
PubMed2001

Midazolam amnesia and conceptual processing in implicit memory.

Prominent theories of implicit memory (D. Schacter, B. Church, & J. Treadwell, 1994) emphasize the dominant role of perceptual processing in mediating priming on perceptual implicit memory tests. Examinations of the effects of conceptual processing on perceptual implicit memory tests have produced ambiguous results. Although a number of investigations (e.g., J. Toth & R. Hunt, 1990) have demonstrated that variations in conceptual processing affect priming on perceptual implicit memory tests, these effects may arise because of the contaminating effects of explicit memory. The current experiment examined this controversy using midazolam, a benzodiazepine that produces a dense, albeit temporary, anterograde amnesia when injected prior to study. The experiment examined whether the effects of generation found on the implicit memory test of perceptual identification were affected by a midazolam injection prior to study. Results demonstrated that midazolam substantially diminished generation effects in free and cued recall, as well as overall performance on these tests, but had no detectable effect on the generation effect in perceptual identification.

Adult↗
PubMed1990

Repetition priming of words and pseudowords in divided attention and in amnesia.

Repetition priming of novel stimuli (pseudowords) and stimuli with preexisting representations (words) was compared in two experiments. In one, 19 normal male subjects performed a lexical decision task with either focused or divided attention. In another, lexical decision performance was compared between 8 male Korsakoff patients and 8 alcoholic control subjects. In control conditions, repetition speeded responses to both stimulus types. Experimental conditions that minimized the contribution of episodic memory to task performance eliminated reaction time priming for pseudowords but not for words. However, in these same conditions, repetition increased the likelihood that pseudowords would be incorrectly classified. These results indicate that preserved repetition priming effects in amnesia do not solely reflect activation of representations in semantic memory.

Alcohol Amnestic Disorder↗
PubMed1987

Anterograde amnesia induced by hyperthermia in rats.

Anterograde amnesia (AA), forgetting of events that occur following a traumatic episode, has recently been demonstrated by using a mild decrease in temperature (hypothermia) as the amnestic agent. However, no data currently exist to indicate if an increase in body temperature (hyperthermia) might affect memory processing in a similar manner. Experiments 1 and 2 demonstrated that increasing the colonic body temperature of the rat to 3-4 degrees C or more above normal during avoidance training produced a significant retention loss when the test occurred 24 hr after training. Slight hyperthermia to 1-2 degrees C above normal did not impair retention. In Experiment 3, AA resulting from an elevation in temperature was reversed by reheating "amnestic" subjects just prior to the 24-hr test. By rapidly reversing hyperthermia immediately after the training trial with a cooling procedure, Experiment 4 demonstrated that hyperthermia-induced AA was not the result of retrograde influences of the heating treatment. Implications of these results are discussed in terms of possible retention deficits which could conceivably follow environmental heat stress or fever hyperthermia resulting from bacterial infection.

Animals↗