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PubMed1977

Protein synthesis and amnesia: studies with emetine and pactamycin.

Two antibiotic inhibitors of protein synthesis, emetine and pactamycin, have been tested for their effects on cerebral and peripheral protein synthesis and amnesia. Peripherally administered emetine but not pactamycin inhibited cerebral protein synthesis, although this inhibition was lower than that observed with cycloheximide or anisomycin. Pactamycin had a lesser effect on adrenal protein synthesis than emetine. This was reflected in the ability of emetine but not pactamycin to block ACTH-induced corticosteroidogenesis. Anisomycin and cycloheximide caused amnesia in a passive avoidance task, whereas pactamycin and emetine did not. These results are inconsistent with the amnesia being due to inhibition of protein synthesis in a peripheral organ. They are also inconsistent with the amnesia being due to the suppression of an adrenocortical response as previously suggested. No obvious correlation between amnesia and the mechanism of protein synthesis was observed. The most parsimonious explanation is that inhibition of cerebral protein synthesis is necessary for amnesia.

Adrenal Glands↗
PubMedDate not supplied

Preventive effect of cholecystokinin octapeptide on experimental amnesia in rats.

The effect of intracerebroventricular (ICV) administration of cholecystokinin octapeptide (CCK-8) on electroconvulsive shock (ECS)-induced amnesia in passive avoidance response was studied in rats. In normal rats, CCK-8 in doses from 1 ng to 1 microgram had no effect on the response when injected before the training trials, immediately after foot shock or before the first retention test. However, proglumide, a CCK-8 receptor blocker, induced marked amnesia when injected in doses from 0.1 to 10 micrograms before the training trials and in doses of 1 and 10 micrograms before the first retention test, though not subsequent to foot shock. ECS given immediately after the foot shock caused amnesia in the 24 hr and 48 hr retention tests, which could have been prevented by CCK-8 injected in doses of 10 ng to 1 microgram prior to the training trials, of 10 ng to 1 microgram following ECS and of 0.1 and 1 microgram before the first retention test. In addition, the effects of CCK-8 and proglumide became pronounced following chronic ICV infusion, using an osmotic minipump, for 7 days at a dose of 1 ng/day and 10 ng/day, respectively. The amnesia induced by proglumide was not affected by arginine vasopressin (AVP), while AVP in doses of 10 ng and 100 ng given 30 min before the training trials prevented ECS-induced amnesia. The antiamnesic effect of AVP was abolished by simultaneous administration of proglumide. On the other hand, AVP-antiserum produced marked amnesia which could be antagonized by CCK-8. However, the antiamnesic effect of CCK-8 was not suppressed by AVP-antiserum.(ABSTRACT TRUNCATED AT 250 WORDS)

Amnesia↗
PubMed1990

Childhood amnesia and distinctions between forms of memory: a comment on Wood, Brown, and Felton.

Recently, Wood and his colleagues (1989) presented a case of childhood amnesia as evidence against the distinction between declarative and procedural memory that has sometimes been applied to human amnesia. Their argument was based on the observation that their patient showed some progress in school over the years, i.e., acquired some declarative knowledge, despite severely impaired day-to-day memory ability. We briefly review their case, together with a carefully studied second case of childhood amnesia not mentioned by Wood et al. Their argument is wrong in several ways. First, the utility of the declarative/procedural distinction for amnesia, or the utility of any other distinction between memory systems, depends on whether or not one kind of memory is impaired selectively, not on the severity of the impairment. In particular there is no requirement that one kind of memory be totally absent. Second, they have not provided the data necessary to support their argument; namely, data showing that the amount of declarative knowledge accumulated during years in school was better than would have been expected given the capacity for moment-to-moment or day-to-day memory. Indeed, the patient's moment-to-moment memory ability is better than represented, and the patient's progress in school was abnormally slow. Third, it is not clear that academic achievement scores provide a direct measure of declarative memory abilities (skill learning and recovery of function may also have contributed). We conclude that the evidence from childhood amnesia is fully consistent with the proposal that amnesia reflects a selective impairment in the formation of long-term declarative memory.

Achievement↗
PubMed2001

Dehydroevodiamine attenuates beta-amyloid peptide-induced amnesia in mice.

Dehydroevodiamine has been reported to have anticholinesterase activity and an anti-amnesic effect. This study examined the effects of dehydroevodiamine on scopolamine- and beta-amyloid peptide-(25--35)-induced amnesia in mice, using a step-through passive avoidance test. Similarly to the cholinesterase inhibitor, physostigmine (0.03--0.3 mg/kg, i.p.), dehydroevodiamine (0.75--12.0 mg/kg, i.p.) administered 30 min before the training trial, immediately after the training trial, and 30 min before the retention test significantly improved scopolamine- and beta-amyloid peptide-(25--35)-induced amnesia. In beta-amyloid peptide-(25--35)-induced amnesia, the rank order of anti-amnesic potency in these three administration schedules for dehydroevodiamine was different from that for physostigmine. Furthermore, dehydroevodiamine was more potent to improve beta-amyloid peptide-(25--35)-induced amnesia than scopolamine-induced amnesia when administered before the training trial. These results suggested that dehydroevodiamine may have an action other than that of an anticholinesterase and may be a novel and effective ligand for improvement of beta-amyloid type amnesia.

Alkaloids↗
PubMed2003

Midazolam amnesia and retrieval from semantic memory: Developing methods to test theories of implicit memory.

Studies of organic anterograde amnesia have been central to the development of theories of implicit memory. Pharmacological amnesia provides an additional method for exploring implicit memory, allowing for the experimental manipulation of amnesia and the testing of more participants. A significant concern with pharmacological amnesia is whether its cognitive effects are specific to explicit memory. The current research examines the effects of the benzodiazepine, midazolam, on retrieval from semantic memory and encoding in explicit memory. We focus on midazolam because it holds significant advantages over other benzodiazepines in inducing pharmacological amnesia and prior research suggests it may be useful for testing theories of implicit memory. Our results demonstrate that midazolam does not impair accuracy of retrieval from semantic categories, even when it produces anterograde amnesia for retrieved category items on a later recall test. These results suggest ways midazolam can be used to help test theories of implicit memory.

Adult↗
PubMed1987

A neuropsychological study of fact memory and source amnesia.

We investigated the ability of amnesic patients to learn new facts (e.g., Angel Falls is located in Venezuela) and also to remember where and when the facts were learned (i.e., source memory). To assess the susceptibility of fact and source memory to retrograde amnesia, patients prescribed electroconvulsive therapy were presented facts prior to the first treatment and were tested after their second treatment. All amnesic patients exhibited marked fact memory impairment. In addition, some amnesic patients exhibited source amnesia (i.e., they recalled a few facts but then could not remember where or when those facts had been learned). Source amnesia was unrelated to the severity of the memory deficit itself, because patients who exhibited source amnesia recalled as many facts as the patients who did not. These results show that the deficit in amnesia includes an impairment in acquiring and retaining new facts. Source amnesia can also occur, but it is dissociable from impaired recall and recognition and appears to reflect difficulty in remembering the specific context in which information is acquired. The findings are discussed in terms of their significance for how memory is organized.

Adult↗
PubMed2000

Latent learning in medial temporal amnesia: evidence for disrupted representational but preserved attentional processes.

Damage to the hippocampus and medial temporal (MT) structures can lead to anterograde amnesia and may also impair latent learning, in which prior exposure to cues affects their subsequent associability. Normally, latent learning may reflect both representational and attentional mechanisms. Prior work has suggested that individuals with MT amnesia have specific deficits in representational processing; thus, latent learning that invokes primarily representational mechanisms might be especially impaired in MT amnesia. The current results provide preliminary confirmation of this prediction. In Experiment 1, a latent learning paradigm expected to invoke representational mechanisms was impaired in individuals with MT amnesia, whereas in Experiment 2, a paradigm expected to invoke other attentional mechanisms was spared in individuals with MT amnesia. This suggests the representational and attentional components of latent learning are dissociable and differentially affected in anterograde amnesia.

Adult↗
PubMed1975

Role of the biogenic amines in the reversal of cycloheximide-induced amnesia.

Amnesia was induced by pretraining injections of cycloheximide (CYC) in a food motivated discrimination reversal task. Magnitude of amnesia varied as a function of the amount of training on both the initial discrimination and the reversal and also as a function of the length of intertrial interval used on both the reversal and the test. Memory spontaneously recovered 48 hr. following reversal training. Recovery from amnesia was induced by pretesting injections of d-amphetamine and 2 monoamine oxidase inhibitors, pargyline and catron. This enhanced performance was a true recovery of the memory and not a result of enhanced learning or increased arousal. Depletion of catecholamines by alpha-methyl-para-tyrosine, a tyrosine hydroxylase inhibitor, and diethyldithiocarbamate, a dopamine beta hydroxylase inhbitor, resulted in an amnesia quantitatively and qualitatively similar to amnesia induced by CYC. These data support the hypothesis that CYC-induced amnesia is mediated via central catecholamines.

Amnesia↗
PubMed1972

Acetoxycycloheximide-induced transient amnesia: protective effects of adrenergic stimulants.

It has previously been shown that rats trained 5 hr after intracerebral injection of acetoxycycloheximide show a transient amnesia at 24 hr after training. We have tested the possibility that adrenergic stimulants might provide protection from the amnesia. Metaraminol, given either before or after training or before testing, prevents the drug-induced amnesia. D-Amphetamine, injected soon after training, also prevents the amnesia. A model is presented to explain the drug-induced amnesia in terms of both the assumed effect of acetoxycycloheximide on the adrenergic system and prevention of the amnesia by metaraminol and D-amphetamine.

Acetates↗
PubMedDate not supplied

Implicit and explicit memory in amnesia: some explanations and predictions by the TraceLink model.

After a brief overview of some of the characteristics and neuroanatomy of amnesia, a new model of amnesia is described: the TraceLink model. One novel aspect of the model is that it makes specific and testable predictions regarding semantic dementia, a recently described disorder that is viewed here as being related to amnesia. The TraceLink model consists of: a trace system (roughly the neocortix), a link system (hippocampus and adjacent areas), and a modulatory system (certain basal forebrain nuclei). Different forms of learning in the TraceLink model are explained, followed by a discussion of implicit and explicit memory, prominence (ease of recall) and persistence (resistance to brain damage), consolidation, and Ribot gradients in retrograde amnesia. Patterns of recovery from retrograde amnesia are also discussed, and novel predictions are derived regarding implicit memory and various forms of amnesia.

Amnesia↗
PubMed2004

Drug-facilitated robbery or sexual assault: problems associated with amnesia.

Amnesia following sedative-hypnotic drug exposure is discussed. Anterograde amnesia clearly occurs with many benzodiazepines. Several drugs are assessed: benzodiazepines and two hypnotics in particular that are structurally unrelated to the benzodiazepines but share some of their properties: zolpidem and zopiclone. The amnesic effects of these drugs are described, memory process, biology of memory, and memory process impairment documented. With these drugs anterograde amnesia has been demonstrated to be dose dependent. This effect is associated with hypnotic drugs, however, the receptors are different. As regards forensic medicine, a significant and specific type of amnesia should be considered: amnesia automatism or amnesic complex automatism. Also, several cases observed in our laboratory are presented to demonstrate the impact of amnesia.

Amnesia↗
PubMed1999

Episodic memory in transient global amnesia: encoding, storage, or retrieval deficit?

OBJECTIVES: To assess episodic memory (especially anterograde amnesia) during the acute phase of transient global amnesia to differentiate an encoding, a storage, or a retrieval deficit. METHODS: In three patients, whose amnestic episode fulfilled all current criteria for transient global amnesia, a neuropsychological protocol was administered which included a word learning task derived from the Grober and Buschke's procedure. RESULTS: In one patient, the results suggested an encoding deficit, and in two others, a storage deficit. CONCLUSIONS: The encoding/storage impairment concerning anterograde amnesia documented in our patients stands in clear contrast with the impairment in retrieval which must underly the retrograde amnesia that also characterises transient global amnesia. This dissociation in turn favours the idea of a functional independence among the cognitive mechanisms that subserve episodic memory.

Aged↗
PubMed1999

Basal forebrain amnesia: does the nucleus accumbens contribute to human memory?

OBJECTIVE: To analyse amnesia caused by basal forebrain lesions. METHODS: A single case study of a patient with amnesia after bleeding into the anterior portion of the left basal ganglia. Neuropsychological examination included tests of attention, executive function, working memory, recall, and recognition of verbal and non-verbal material, and recall from remote semantic and autobiographical memory. The patient's MRI and those of other published cases of basal forebrain amnesia were reviewed to specify which structures within the basal forebrain are crucial for amnesia. RESULTS: Attention and executive function were largely intact. There was anterograde amnesia for verbal material which affected free recall and recognition. With both modes of testing the patient produced many false positive responses and intrusions when lists of unrelated words had been memorised. However, he confabulated neither on story recall nor in day to day memory, nor in recall from remote memory. The lesion affected mainly the nucleus accumbens, but encroached on the inferior limb of the capsula interna and the most ventral portion of the nucleus caudatus and globus pallidus, and there was evidence of some atrophy of the head of the caudate nucleus. The lesion spared the nucleus basalis Meynert, the diagnonal band, and the septum, which are the sites of cholinergic cell concentrations. CONCLUSIONS: It seems unlikely that false positive responses were caused by insufficient strategic control of memory retrieval. This speaks against a major role of the capsular lesion which might disconnect the prefrontal cortex from the thalamus. It is proposed that the lesion of the nucleus accumbens caused amnesia.

Amnesia↗
PubMed2005

The influence of central administration of dopaminergic and cholinergic agents on morphine-induced amnesia in morphine-sensitized mice.

In the present study, effects of intracerebroventricular (i.c.v.) injections of dopaminergic and cholinergic agents on morphine-induced amnesia in morphine-sensitized mice were investigated by using a one-trial passive avoidance task. Amnesia induced by pre-training morphine was significantly reversed in morphine-sensitized mice, which had previously received once daily injections of morphine (20 and 30 mg/kg, s.c.) for 3 days. Three daily injections of SKF 38393 (1, 2 and 4 g/mouse, i.c.v.) or SCH 23390 (0.25, 0.5, 0.75 and 1 g/mouse, i.c.v.) before morphine, and during morphine-sensitization, decreased and increased the amnesia induced by pre-training morphine respectively. Three daily injections of quinpirole (0.3, 1 and 3 g/mouse, i.c.v.) or sulpiride (0.03, 0.1, 0.3 and 1 g/mouse, i.c.v.) before morphine, also decreased and increased the amnesia induced by pre-training morphine respectively. Morphine-sensitized mice received similar injections of cholinergic agents. Three daily injections of physostigmine (1, 3 and 5 g/mouse, i.c.v.) or atropine (1, 4 and 7 g/mouse, i.c.v.) before morphine, and during morphine-sensitization, decreased and increased the amnesia induced by pre-training morphine respectively. Three daily injections of nicotine (0.75, 1 and 2 g/mouse, i.c.v.) or mecamylamine (1, 3 and 6 g/mouse, i.c.v.) before morphine, also decreased and increased the amnesia induced by pre-training morphine respectively. The results suggest that morphine sensitization affects the impairment of memory formation and thus it is postulated that central dopaminergic and cholinergic systems may play an important role in this effect.

Amnesia↗
PubMed1985

[Pharmacological studies on sufoxazine (Y-8894). (I) Effects on experimental amnesia in mice].

The effects of sufoxazine on various experimental amnesia models were studied using passive avoidance behavior in mice. Sufoxazine had no influence on learning and memory in intact mice. Sufoxazine, administered either immediately after CO2 exposure or 30 min prior to the acquisition trial, improved CO2 induced amnesia. It also improved both electroconvulsive shock (ECS) induced amnesia (administered immediately after the amnestic treatment) and scopolamine induced amnesia (administered immediately after the acquisition trial). The anti-depressant drugs, imipramine and desipramine had no ameliorative activity in any of these experimental amnesia models. These results suggest that sufoxazine improves amnesia experimentally induced by various methods.

Amnesia↗
PubMed1984

Beneficial effect of idebenone (CV-2619) on cerebral ischemia-induced amnesia in rats.

An experimental model of amnesia induced by cerebral ischemia after one-trial passive avoidance learning was established to test the effects of a novel compound, 6-(10-hydroxydecyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone (idebenone, CV-2619), and some commonly used drugs in rats. One day after the vertebral artery was electrocauterized bilaterally, the common carotid artery was transiently occluded bilaterally to produce cerebral ischemia. The amnesia was estimated by the response latency for a rat to step from a light safety compartment to a dark compartment in which a foot-shock was given. The results of the retention test given 24 hr after the ischemia indicated that amnesia was successfully produced when the 200-600 sec ischemia was provided within 20 min after the avoidance learning. The effects of drugs on the amnesia induced by a 200-sec ischemia immediately after the avoidance learning were as follows: CV-2619 (10, 30 mg/kg, i.p. or p.o.) given before the retention test significantly increased the response latency, indicating a reversal effect on the amnesia. Physostigmine (0.1, 0.2 mg/kg, i.p.) and arginine-vasopressin (10 micrograms/kg, s.c.) were also effective, and calcium hopantenate (500 mg/kg, p.o.) showed a slight reversal action. Furthermore, CV-2619 (10 mg/kg, i.p.), given before or after the ischemia, significantly inhibited the appearance of amnesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Amnesia↗
PubMed1975

[Transient global amnesia - a paroxysmal amnestic syndrome (author's transl)].

The Syndrome of Transient Global Amnesia is clinically characterized by a disorder of the ability to form memory engrams, appearing suddenly and lasting for several hours. Since the first papers on this syndrome by Bender (1956) and Fisher and Adams (1964) approximately one hundred cases of transient global amnesia have been described. Symptomatology, course, somatic findings and differential diagnosis are discussed with consideration of the literatur and three own observations. Regarding the etiology most authors discuss a transitory localized ischemia in the circulatory area of the vertebral-basilar artery system. Relapsing episodes occur less frequently than single episodes. In connection with this disorder characterized by the paroxysmal occurence and the episodic course, possible ways of genesis of amnesic syndromes are discussed. Theoretically three types of amnestic syndromes of organic origin may be differentiated: (1) amnesia in the frame of "function psychosis", i.e. of global mental deterioration caused by various diffuse brain function disorders; (2) amnesia caused by a combination of diffuse (function psychosis) and local brain function disorder; (3) purely local type of amnesia without function psychosis. In the combined type of amnesia a dissociation between the severity of memory disorders and relatively mild function psychosis is to be found. The importance of psychopathometric investigations, i.e. of quantitative determination of other mental dysfunctions besides memory disorder, for the interpretation of an amnesic syndrome is emphasized. Unfortunately these have not been possible in the cases described in this paper.

Adult↗
PubMedDate not supplied

[Transient global amnesia. Case report].

All memory disturbances, especially those developing suddenly, cause anxiety of the patient. Transient global amnesia is a form of amnesia of interest in many aspects. The amnesia was described in 1964 by Fisher and Adams, and as yet about 1000 cases have been reported. Middle aged or elderly patients prevail. The attack of amnesia lasts from several to about 20 hours and begins suddenly being regarded as mental confusion. The amnesia covers recent and remote events in many years. During the attack the patient is not appearing to be ill, but is depressed not knowing what has happened. The awareness of own personality, the ability to solve logical problems and visuospatial functions are preserved. The ability to execute complex activities, e.g. car driving, is normal. The aetiology of the disorder is completely unknown. The hypotheses for explaining the syndrome are: 1. ischaemia in the posterior cerebral arteries region with transient fall of blood supply through the vertebrobasilar system, 2. epilepsy or migraine, 3. disturbed aggregation of platelets in the cerebral vessels leading to loss of vessel patency. The first hypothesis seems least plausible. Attacks of this amnesia were noted after triazolam, after thalamic infarction and cerebral angiography, in brain tumours, hydrocephalus, scleroderma, frontal lobe haemorrhage. After an attack the events occurring in it are not remembered. Recurrence of attacks is very rare. Most authors consider that the disorder is benign and regresses without sequelae or only with slight changes in cognitive functions and memory fixation.

Age Factors↗