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At least 19 recordsLinked to original sources

PubMed1979

Pituitary hormones and amnesia.

Pituitary hormones profoundly influence behavior through direct actions on the brain. One of these behavioral effects is the attenuation of experimental amnesia. Traditionally, amnesia is considered as a "loss of memory." Memory comprises at least 2 stages: input (memory consolidation) and output (memory retrieval). Theoretically, disturbance of either aspect of memory may be the cause of amnesia. Also, it is possible that amnesia is based on a factor or factors not related to memory. Data and theories on amnesia in man were reviewed. Some salient features were mentioned: (1) amnesia can be induced by a variety of agents; (2) amnesia covers periods ranging from seconds to years; (3) amnesia gradients can be established; (4) amnesia is to a large extent reversible. From this survey, it seems possible that amnesia is not a homogeneous phenomenon and that even in one person a disturbance of both memory consolidation and memory retrieval may be produced by one and the same event. Animal studies in general have confirmed these conclusions. We have developed an animal model in order to study the effects of pituitary peptides on amnesia. This model is based on CO2-induced amnesia for a one-trial passive avoidance response in rats. This amnesia could be attenuated by treatment with ACTH-analogs 1 hour before the retrieval test. This anti-amnesic effect of ACTH-analogs was not dependent on the nature of the behavioral response or the amnesic treatment. The vasopressin-analog DGLVP similarly exerted an anti-amnesic effect when injected before the retrieval trial. In contrast to ACTH-analogs, however, it also reduced the amnesia when injected before acquisition. These results suggest that amnesia may comprise a "faulty-consolidation" and a "faulty-retrieval" component, which may be amended by different pituitary hormones. The study of the anti-amnesic activity of peptides therefore not only serves to characterize the nature of the behavioral effect of these peptides but may also prove to be helpful of the unraveling of processes involved in amnesia.

Adrenocorticotropic Hormone↗

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↗

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↗

PubMed1978

Conscious sedation with intravenous drugs: a study of amnesia.

A comparison of amnesia that is produced by two intravenous sedation techniques commonly used to reduce anxiety in ambulatory oral surgery patients showed that both techniques induce high levels of safe, predictable amnesia. More than 200 patients undergoing surgical extraction of third molars were asked to verbally identify visual and cutaneous-tactile stimuli intraoperatively. The patients responded via written questionnaires at the postoperative interview sessions. No retrograde amnesia was observed. Complete amnesia was attained for the local anesthetic injections. Amnesia for visual stimuli was significantly lower than for cutaneous-tactile stimuli. No significant differences in amnesia were observed between the two drug combinations studied.

Adult↗

PubMed1977

Effects of d-amphetamine and strychnine on cycloheximide- and diethyldithiocarbamate-induced amnesia in mice.

Groups of C57BL/6J mice were administred cycloheximide (CYC) 30 min before or immediately after training on a passive avoidance task and tested 72 hr later. Some CYC-pretreated groups were given strychnine or d-amphetamine (d-amp) immediately after training and others were given d-amp 1 hr after training. Other groups were given diethyldithiocarbamate (DDC) at various times before or after training. Some DDC-pretreated groups were gived-amp or strychnine as described above for CYC groups. Immediate posttraining administration of 5 mg/kg d-amp, but not strychnine, prevented amnesia in CYC-pretreated mice. The DDC induced an apparent amnesia when administered from 30 min before training to 3 hr after training. Posttraining administration of d-amp or strychnine did not prevent DDC-induced amnesia. These results are discussed in relation to previous suggestions that CYC- and DDC-induced amnesia may be the result of a functional impairment of catecholamine neurotransmitter systems by these drugs.

Amnesia↗

PubMed1978

Retrograde amnesia produced by several treatments: evidence for a common neurobiological mechanism.

This experiment examined the effects on memory of various amnestic treatments in animals earlier treated with the alpha-adrenergic antagonist phenoxybenzamine (PBZ). Thirty minutes before being trained in a one-trial inhibitory (passive) avoidance task, animals received an injection of PBZ or saline. Immediately after training, each animal received one of the following amnestic treatments: stimulation of the frontal cortex or amygdala, pentylenetetrazol, diethyldithiocarbamate, or cycloheximide. In control animals, each treatment produced retrograde amnesia. However, PBZ-treated animals did not develop amnesia. These findings suggest that there may be a common neurobiological mechanism underlying the amnesias produced by many treatments.

Amnesia↗

PubMed1977

Some characteristics of amnesia induced by FLA-63 an inhibitor of dopamine beta hydroxylase.

The amnesic effects of FLA-63, a potent dopamine-beta-hydroxylase (DBH) inhibitor, were investigated in a food motivated spatial discrimination task. Groups of C57BL/6J mice were injected with either 5 mg/kg, 15 mg/kg, 25 mg/kg, 35 mg/kg or physiological saline 4 hr prior to training. Amnesia was observed 24 hr following training at all dose levels except 5 mg/kh. The performance deficit was specific to memory of the discrimination and not the result of state-dependency. Training conditions which produce an increase in habit strength prevented the amnestic effects of FLS-63. Spontaneous recovery of memory occurred 48 hr following drug administration. Recovery from amnesia was also induced by injections of a monoamine oxidase inhibitor, pargyline, administered 2 hr prior to the retention test. These data suggest that amnesia induced by norpinephrine (NE) depletion is the result of impairment of mechanisms necessary for memory retrieval.

Amnesia↗

PubMed1975

Effect of age of habit on susceptibility to cycloheximide-induced amnesia in mice.

The amnesic effects of cycloheximide (CYC) on habits of different ages were investigated in a food-motivated, discrimination-reversal task. Groups of C57BL/6J mice were injected 30 min before training or immediately, 3 days, 6 days, or 9 days after training. Retention was tested 24 hr after CYC treatment. The usual amnesic effect of CYC occurred in animals injected before training. No amnesia was apparent in groups injected immediately, 3 days, or 9 days after training. However, a reliable and reproducible amnesia occurred in the group injected 6 days after training. This amnesia could be reversed by pretest treatment with a monoamine oxidase inhibitor, pheniprazine. Pheniprazine, given 7 days after training, also enhanced retrieval of memory in saline-injected mice.

Amnesia↗

PubMed1978

The neuroanatomy of amnesia. A critique of the hippocampal memory hypothesis.

The discovery that medial temporal lobe lesions produce amnesia in humans if the lesion extends sufficiently far posteriorly to include the hippocampus forms the keystone of the hippocampal memory hypothesis. Strong supporting evidence comes from the occurrence of mammillary body disease in Korsakoff's psychosis. Disease of the posterior cerebral artery confirmed the observations on the medial temporal lobectomies by showing that pathology in the ventromedial quadrant of the temporal lobe produces amnesia. The occasional piece of contradictory evidence was sufficiently ambiguous to be dismissed or re-interpreted. Although the contradictory evidence that emerged from animal research created severe difficulties, opinion had crystallized on the matter to the degree that the data were unable to force rejection of the hippocampal memory hypothesis. This necessarily led to the conclusion that the animal model is a poor one: either the human hippocampus is unique with respect to memory or the tests which are used in animals do not tap the same mnemonic processes that are impaired by the human lesions. Both these arguments are nearly impossible to refute. The brain of every species is different and there is no way in which monkeys and humans can be tested under identical conditions. There has never been much enthusiasm for the suggestion that the human hippocampus is so different from other animals that this uniqueness could account for the apparent differences between the behavioural effects of human and animal hippocampal lesions. However, many experimenters have devised clever tests of the possibility that the problem is in the animal behavioural measures. Given sufficient circularity of reasoning, the project must necessarily eventually be successful. The argument is that if the usual tests of learning and memory that are used with animals are not disrupted by hippocampal lesions, then these are not tests of the kinds of learning and memory defects displayed by human amnestics. One has only to search for tasks that are disrupted by hippocampal lesions in animals, and these then must tap the same memory processes that are disrupted by the human lesions. The possibility has rarely been seriously considered that it might be damage to some structure in the ventromedial quadrant of the temporal lobe other than the hippocampus that is responsible for the amnesia. The amygdala and entorhinal area have been ruled out by both the human and animal data. However, the temporal stem is a likely possibility. Its position makes it vulnerable to the surgical approach which was used in human medial temporal lobectomies, and its damage in animals produces deficits in learning and retention. When medial temporal lesions were made in monkeys in the same way that they were made in humans, inadvertent damage to the temporal stem occurred along with the intended amygdaloid and hippocampal injury. Symptoms characteristic of damage to the temporal cortex resulted from these lesions and they were probably caused by the damage to the stem...

Alcohol Amnestic Disorder↗

PubMed1977

Respiratory effects and amnesia after premedication with morphine or lorazepam.

Lorazepam, a new benzodiazepine, was compared with morphine for premedication. Ten patients received morphine 10 mg/70 kg i.m. and 10 received lorazepam 4 mg/70 kg i.m. Respiratory effects were assessed from the change in slope (S) and intercept (B) of the carbon dioxide response line, using a development of Read's rebreathing method. Morphine depressed S by 47% (P less than 0.01), but after lorazepam S increased by 27% (P less than 0.05), neither drug altering B significantly. In two volunteers lorazepam was assessed by both the rebreathing and the steady-state methods; after lorazepam S was smaller by the steady-state than by the rebreathing technique. The findings for lorazepam are consistent with the known effects of sleep on carbon dioxide sensitivity. Amnesia lasting 4-8 h occurred in all patients who received lorazepam so that pain and nausea during this period were not recalled, but no patient who received morphine experienced amnesia. We conclude that lorazepam merits further study, particularly where sedation without respiratory depression is needed, as in obstetrics, and where amnesia for uncomfortable procedures is required.

Adolescent↗

PubMed1979

[Flunitrazepam with anterograde amnesia and reduction of blood pressure before local anaesthesia without intubation in 3000 ENT operations (author's transl)].

After premedication with flunitrazepam=Rohypnol 2 mg orally (2--3 hours preop.) and morphine-atropine (30 min preop.) the patient receives slowly "Ro" i.v. until the phenomenon of volume reduction when speaking is observed. This allows for the smallest possible dosis to achieve sufficient amnesia. After about 20 min the patient becomes responsive again, while his amnesia lasts for about 3 hours more. The cardiovascular functions remain stable with a 25% decrease of systolic blood pressure. Vomiting is reduced. The dry operative field makes microsurgery much easier and improves the final result of the operation. After gaining sufficient experience of the staff, 100% amnesia was achieved in all operations during the last 3 months.

Administration, Oral↗

PubMed1976

DDC-induced retrograde amnesias prevented by injections of dl-DOPS.

Injection of a dopamine beta-hydroxylate inhibitor, diethyldithiocarbamate (DDC) in rats 30 min prior to training of a step-down passive avoidance task impaired performance of the task 24 hr later. Similarly, injection of DDC 30 min prior to testing blocked retrieval of a passive avoidance habit trained in normal rats the previous day. Injection of a direct norepinephrine (NE) precursor, dl-thero 3,4-dihydroxyphenylserine (DOPS) 60 min before DDC prevented both amnesias. These data support the hypothesis that reduced levels of NE are responsible for DDC-induced amnesias.

Amnesia, Retrograde↗

PubMed1979

Peripheral catecholamines and memory: characteristics of syrosingopine-induced amnesia.

The effect of syrosingopine on retention of a passive avoidance trial in mice was investigated. The drug given in doses of 2.5, 4.0 or 6.0 mg/kg 2 hr before training, but not when given 24 or 0.5 hr or immediately after training, resulted in amnesia 7 days later. Dopamine or norepinephrine administered systemically 15 min before to 10 min after training was able to block the syrosingopine-induced amnesia. The role of peripheral catecholamines in memory formation was discussed.

Amnesia↗

PubMed1979

Clonidine reverses the amnesia induced by dopamine beta hydroxylase inhibition.

The role of noradrenergic (NE) mechanisms in amnesia induced by the dopamine-beta-hydroxylase (DBH) inhibitor, diethyldithiocarbamate (DEDTC) was examined by studying the antiamnestic characteristics of the alpha-NE receptor stimulator clonidine. DEDTC (250 mg/kg) administered 3 hr prior to training to C57BL/6J mice resulted in marked deficits when retention of a multiple trial food motivated spatial discrimination task was measured 24 hr after learning. Investigation of the temporal aspects of recovery indicated that the agonist was an effective antiamnestic agent when administered 0, 1, 3, 21 and 23 hr after training. No recovery was observed when the drug was administered 6 and 18 hr posttraining. A dose response study of the effectiveness of clonidine administered 1 hr prior to testing indicated recovery of memory at doses ranging from 10-500 microgram/kg. The clonidine induced recovery was not a result of general performance facilitation, but specific to the memory tested. In addition, the clonidine effect was pharmacologically specific to its actions on NE receptors, as recovery was blocked by pre-treatment with the alpha-NE antagonist, phentolamine. No recovery from DEDTC induced amnesia was seen with post-training or pre-test injection of d-amphetamine.

Amnesia↗

PubMed1979

Transient global amnesia after clioquinol: five personal observations from outside Japan.

Five personal observations of an acute amnestic episode in younger individuals after intake of clioquinol are described together with three observations from the medical literature. In five of these cases the episode began after an unusually large dose, in three after a therapeutic one with a latency of about 24 hours. The clinical aspect closely resembled classical transient global amnesia but the episode after clioquinol lasted longer (24 hours to three days) and a more or less extensive retrograde amnesia persisted permanently. In one patient after three tablets of Mexase a clioquinol concentration of 12 microgram/ml in plasma was found 24 hours after the specified dose, which is an unexpectedly high concentration compared to those reported as late as 24 hours after a single equal dose of Mexase or any other clioquinol-containing preparation. Another patient had a brief relapse two years after the first episode, after a single therapeutic dose of another clioquinol preparation.

Adult↗

PubMed1976

Reversal of amnesia by an orally active ACTH 4-9 analog (Org 2766).

The ACTH 4-9 analog, H-Met((O2)-Glu-His-Ph-D-Lys-Phe-OH (Or 2766), attenuates in rats CO2-induced amnesia for a one-trial passive avoidance step-through response when administered prior to the retrieval test but not when given prior to acquisition. Even a dose of 0.001 mug/rat Org 2766 yields an anti-amnesic effect. In this respect Org 2766 is more active than the ACTH fragment ACTH 4-10. An anti-amnesic effect was also obtained when Org 2766 was administered orally. ACTH 4-10 (100 mug/rat) has to be given SC within 8 hr of the retrieval test in order to be effective. A similar time span of effectiveness was observed when Org 2766 was SC injected in a dose of 0.1 mug/rat. The anti-amnesic effect of ACTH 4-10 remains when the time interval between acquisition and retrieval is extended beyond the usual 24 hr. The same appeared to be true for SC ADMINISTERED Org 2766. It is suggested that ACTH-like peptides, and particularly the orally active Org 2766, may be helpful in the treatment of deficient mental performance.

Administration, Oral↗

PubMed1979

Recurrent transient global amnesia in a case with cerebrovascular lesions and livedo reticularis (Sneddon Syndrome).

Eight attacks of transient global amnesia were observed in a female patient who suffered from livedo reticularis and a series of other neurological symptoms, which were transient in most stances. The neurological deficits include focal epileptic attacks, unilateral loss of vision, paresis of left arm and/or leg and dysarthria. The first amnestic attack was seen at the age of 19. The episodes lasted from a few to 3 days. The intervals between the amnestic episodes varied between a few days and 11 years. The livedo reticularis became more obvious during each neurological episode and was less pronounced during the time of remission. A benign type of essential hypertension and parproteinemia (gamma-M) was found. The investigations failed to show any evidence of essential thrombocythemia, polyarteriitis nodosa, lupus erythematodes and other immune complex diseases. The underlaying disease remained unclear.

Amnesia↗

PubMed1978

Effect of age on amnesia and sedation induced by flunitrazepam during local anaesthesia for bronchoscopy.

Bronchoscopy was undertaken in 79 outpatients using local anaesthesia plus an i.v. injection of flunitrazepam 0.01 mg kg-1. The co-operation of the patients and the ease of bronchoscopy were good regardless of the age of the patient. There was an increase in amnesia for the bronchoscopy with increasing age, but the most distinct difference between different age groups was that the amnesic action of flunitrazepam was evident earlier and persisted longer in patients of more than 60 yr. Eye co-ordination and ability to stand steadily and walk on a line returned to normal more slowly in patients more than 60 than in those less than 60 yr, but no differences in recovery were noted between patients less than 40 and those of 40--59 yr, or between those 60--69 and those more than 70 yr.

Adult↗