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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↗
PubMed1978

Studies on memory: spontaneous return of memory in 6-hydroxydopamine-treated mice and its relation to cycloheximide-induced transient amnesia.

We suggested previously that cycloheximide-induced transient amnesia was due in part to side-effects of the antibiotic on the central adrenergic system at the time of testing and that spontaneous return of memory depended upon recovery of the adrenergic system. To test these possibilities, mice chronically depleted of brain catecholamines (CAs) by 6=hydroxydopamine (6-OHDA) were trained in an avoidance-discrimination task and tested for spontaneous return of memory. Contrary to our hypothesis, amnesia at 24 hr after training was followed by recovery of memory by 72 hr, which indicates that recovery of memory can occur independently of adrenergic recovery. Injection of alpha-methyl-para-tyrosine immediately after training prevented return of memory at 72 hr, suggesting that the residual CAs remaining after 6-OHDA are necessary for memory to spontaneously return at this time.

Amnesia↗
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↗
PubMed1980

Studies of memory: a reevaluation in mice of the effects of inhibitors on the rate of synthesis of cerebral proteins as related to amnesia.

Tests were made of the postulates stating that the degree of inhibition of protein synthesis either (a) at training or (b) following training is the critical variable that determines the degree of amnesia. As a first step it was found that the concentrations of numerous cerebral amino acids were substantially increased in 2 strains of mice 0.5 hr after treatment with amnesic doses of the inhibitors of protein synthesis, cycloheximide (CXM) and anisomycin. This observation led, in several different experiments, to a comparison of the apparent degree of inhibition of protein synthesis derived from the acid-soluble radioactivity with that derived from the specific radioactivity of tyrosine tagged with L(1-14C)-tyrosine. In all instances the apparent degree of inhibition was decreased when based upon tyrosine's specific radioactivity. The effect of several treatments with CXM on memory of a 1-trial passive avoidance task provided data for analysis of the relationship between the degrees of amnesia and those of the more accurate estimates of inhibition of protein synthesis based upon the specific radioactivity of tyrosine. The results failed to support the views that the level of inhibition of protein synthesis at or after training are entirely sufficient to account for the behavioral rr indirect change in the brain that antagonizes the amnesic effects of the antibiotic and that consequently contributes to the survival of memory in mice trained 2 hr after a large amnesic dose of CXM.

Amino Acids↗
PubMed1988

Specificity of piracetam's anti-amnesic activity in three models of amnesia in the mouse.

The effects of piracetam on the amnesias induced by scopolamine, diazepam and electroconvulsive shock (ECS) were studied in a passive avoidance procedure in the mouse and compared with the interactions of piracetam with the major behavioral effects of these treatments, namely scopolamine-induced hyperactivity, diazepam-induced release of punished behavior (Four Plates Test) and ECS-induced convulsions. Amnesia was induced by injecting scopolamine or diazepam (1 mg/kg, IP) 30 minutes before or applying ECS immediately after the first session (S1) of the passive avoidance task. Piracetam was studied at 3 doses (512, 1024 and 2048 mg/kg) administered PO 60 minutes before S1. Retention was measured 24 hours later (S2) in the absence of any treatment. Piracetam dose-dependently attenuated the memory deficits induced by the three amnesic treatments but did not affect either scopolamine-induced hyperactivity, diazepam-induced release of punished behavior or ECS-induced convulsions. These results point to the specificity of piracetam's anti-amnesic activity and, in particular, suggest that piracetam can suppress the memory disturbances induced by diazepam without affecting diazepam's anxiolytic activity. The test battery employed would therefore seem highly suitable for evaluating the potential nootropic activity of novel compounds.

Amnesia↗
PubMed1988

Alleviation of scopolamine amnesia by different retrieval enhancing treatments.

Mice were trained in a one-way active avoidance task to a criterion of 9/10 avoidances. Immediately following training they were injected with scopolamine hydrochloride (1 mg/kg SC) or with saline. Retention was assessed 3 days after training by 5 test trials on which the UCS was not present. Thirty min prior to the test, groups were injected with different doses of arecoline, d-amphetamine sulphate or with saline. Other scopolamine-treated mice were exposed to the CS or the UCS 24 hr prior to the test. The scopolamine-induced amnesia was attenuated by both 0.5 and 1.0 mg/kg arecoline and by 2.0 mg/kg d-amphetamine. Retention was also improved by exposure to the CS and the UCS. These data show that scopolamine amnesia can be alleviated by treatments which activate retrieval processes.

Amnesia↗
PubMed1991

Effect of a new cognition enhancer, alpha-glycerylphosphorylcholine, on scopolamine-induced amnesia and brain acetylcholine.

The present study investigates the effect of the administration of alpha-glycerylphosphorylcholine (alpha-GPC) on scopolamine-induced amnesia and on brain acetylcholine (ACh) levels and release in rats. The results indicate that alpha-GPC, when administered orally, reverses the amnesia caused by scopolamine in passive avoidance. The peak effect is observed using 600 mg/kg IG, 5 h before training. The effect of the drug is long lasting (up 30 h) in accordance with its pharmacokinetic characteristics. Since, alpha-GPC administered IG is cleaved within the gut mucosal cells to glycerophosphate and free choline, it is tempting to speculate that this drug acts by increasing the ACh precursor pool. This view is supported also by the observation that alpha-GPC partially counteracts the decrease of brain ACh levels elicited by scopolamine administration. The effect is observed in the hippocampus and cortex, but not in the striatum. Moreover, in ex vivo experiments, alpha-GPC is able to increase the amount of ACh released by rat hippocampus slices following potassium stimulation.

Acetylcholine↗
PubMed1991

The effects of atrial natriuretic peptide on electroconvulsive shock-induced amnesia in rats. Transmitter-mediated action.

Electroconvulsive shock (ECS) applied immediately after passive avoidance learning in rats caused partial amnesia. This could be prevented by administering r-ANP into the lateral brain ventricle. The effects of pre-treatment with different receptor blockers: (haloperidol, atropine, phenoxybenzamine, propranolol, naloxone, bicuculline and methysergide) on the ANP-induced antiamnesia were investigated. The receptor blockers per se in the doses selected had no influence on the ECS-induced amnesia. Haloperidol, atropine and propranolol blocked the antiamnestic action of the peptide, while phenoxybenzamine, naloxone, bicuculline and methysergide were ineffective. The results confirm our previous observations that ANP might play a role in learning and memory processes and also suggest that the antiamnestic action of the peptide is mediated by dopaminergic, cholinergic and beta-adrenergic mediator systems.

Amnesia↗
PubMed1983

Transient global amnesia.

The syndrome of transient global amnesia (TGA) is defined and described. Characteristic features, epidemical data, variables possibly provoking TGA, its possible etiology and anatomical basis are reviewed. A transient disturbance in the formation of lasting new memories (usually of less than one day) and a retrograde amnesia (which includes the period of the attack and possibly a short time before) are considered as the main features of TGA. A further trait of TGA is the high age of most of the patients subjected to it (58 years on the average). TGA most likely is based on a transient change in the blood supply of certain regions of the brain. The mechanism by which this change happens is still hypothetical. Regions of the limbic system, in particular the area of the temporal lobe and the hippocampal formation, appear to be affected most likely. Uncertain are: the existence of factors provoking the outbreak of an amnesic attack, the likeliness of multiple episodes of TGA and the neuropsychological alterations in patients who suffered a transient global amnesic attack. The outcome of this review suggests, however, that the incidence of recurrent attacks of TGA is higher than previously assumed and that a transient global amnesic attack may be followed by lasting behavioral deteriorations.

Aged↗
PubMed1986

Step-down-type passive avoidance- and escape-learning method. Suitability for experimental amnesia models.

A method for evaluating passive avoidance- and escape-learning responses simultaneously has been developed for the study of learning and memory in mice. Prolongation of the step-down latency and shortening of the escape latency in the retention test depended on the strength of the voltage of the electric shocks delivered during the training test. Therefore, the step-down latency and escape latency may be good parameters of learning and memory performance. By cycloheximide treatment immediately after training, the step-down latency and escape latency were shortened and prolonged, respectively, in a dose-related manner, and the relationship between the step-down latency and escape latency was significant. Treatment with cycloheximide within 30 min after training caused significant amnesia, but not after more than 60 min. Furthermore, amnesic action of cycloheximide developed 24 hr after the treatment, but not within 4 hr. On the other hand, the step-down latency and/or the escape latency in the training test were changed by pretreatment with diethyldithiocarbamate and scopolamine. Therefore, the amnesic action of these drugs administered before the training should be investigated in detail. The present method, simultaneously estimating passive avoidance- and escape-learning responses, may be useful for the development of experimental amnesia models.

Amnesia↗
PubMed1989

Anisomycin and amnesia in the chick: state-dependent effects are not present with intracranial injections.

It has recently been suggested that intraperitoneal (IP) injection of anisomycin (ANI) in the chick produces amnesia for a one-trial passive avoidance task in a state-dependent manner. We have examined the behavioral and biochemical effects of IP and intracranial (IC) injections of ANI in chicks trained on a one-trial passive avoidance task. IC injection of ANI produced 35% brain protein synthesis inhibition whereas IP injection produced only negligible amounts of protein synthesis inhibition in the brain. IC injection of ANI produced amnesia and was not state-dependent. Patterns of behavior consistent with state-dependent effects were produced by IP injection of ANI. These experiments indicate that there are differences in the pattern of results produced by IP and IC injection of ANI and support the hypothesis that the expression of long-term memory in chicks is associated with protein synthesis.

Amnesia↗
PubMed1995

Memory and amnesia.

Brain damage can cause several distinct disorders of explicit memory as well as several disorders of implicit memory. Organic amnesia is the best studied explicit memory disorder. It is a syndrome that can be caused by lesions in (a) the medial temporal lobes, (b) the midline diencephalon, or (c) the basal forebrain. It remains unresolved whether one or several functional deficits underlie the syndrome, how these deficits should be characterised, and what is the exact location of the causal lesions. There is good evidence that amnesics encode information normally so their deficit(s) must be of storage or retrieval processes. If storage is disrupted, then one would expect item-specific implicit memory for certain kinds of novel information to be disrupted in amnesics. Current evidence is unable to indicate conclusively whether or not this prediction is met mainly because indirect memory test performance depends on explicit as well as implicit memory. Storage deficits should also result in accelerated forgetting in amnesic patients. Studies are described which reveal accelerated loss of free recall, but not recognition, for stories and semantically organised word lists in amnesics at delays between 15 s and 10 min. This suggests that amnesia involves a storage deficit for complex contextual associations that possibly occurs in conjunction with one or more other functional deficits.

Amnesia↗
PubMed1995

Detecting simulated amnesia with event-related brain potentials.

Two experiments were done in which groups of normal college undergraduate subjects were instructed to simulate autobiographical amnesia related to head injury. The subjects were tested for autobiographical knowledge with pencil-and-paper recall and recognition tasks, and on another day, with recognition tasks in which event-related potentials were recorded in response to the same autobiographical items, this time presented on a display screen. In the first study, three Event-Related Potential (ERP) block types were utilized: 1) a block in which the subject's birthdate was an oddball with p = 0.11 and other dates (not relevant to the subject) had p = 0.89, 2) a block in which phone numbers were used as stimuli, and 3) a block in which (mothers' maiden) names were used as stimuli. Only birthdate blocks were used in the second study. A P300 ERP was seen in response to rare, personally relevant items. In both studies, the main effect of stimulus type (personally relevant versus not personally relevant) on P300 amplitude was significant (p < 0.0001) and there was no main effect of block type in the first study. Under a sophisticated malingering instruction set, about 15% of the items were correctly recalled and about 50% were correctly recognized by simulators in pencil-and-paper tests. Under a naive malingering instruction set, most simulating subjects failed to recall and recognize autobiographical items. In the first study, an arbitrarily but a priori derived discrimination criterion based on a subject's average P300 amplitude afforded 92% correct discrimination of simulating individual subjects for birthdates and phone numbers. The value was 77% for mothers' maiden names. The same criterion applied to the single birthdate block in the second study yielded 93% correct discrimination. The results suggest the P300 may be useful in detection of malingered amnesia.

Amnesia↗
PubMedDate not supplied

The effect of beta-(Tyr9)melanotropin-(9-18) on active avoidance behavior, electroconvulsive shock-induced amnesia and T-discrimination learning of rats.

The effect of beta-(Tyr9)melanotropin-(9-18) was investigated on active avoidance behavior, electroconvulsive shock (ECS)-induced amnesia and T-discrimination learning in rats. The decapeptide inhibited the extinction of active avoidance behavior. It was also able to block ECS-induced amnesia if the treatment was performed immediately, or 4 hr or 20 hr after the ECS. In the T-discrimination paradigm the peptide facilitated spatial discrimination learning and reversal learning. These results suggest that beta-(Tyr9)melanotropin-(9-18) can influence learning and memory processes in different behavioral tests.

Amnesia↗
PubMedDate not supplied

Methanesulfonyl fluoride (MSF) blocks scopolamine-induced amnesia in rats.

Cholinesterase inhibitors, such as physostigmine and tetrahydroaminoacridine, have been found to alleviate some of the memory deficits characteristic of senile dementia of the Alzheimer's type (SDAT). Many toxic side effects, however, have been associated with the use of these compounds. Recently, a cholinesterase inhibitor, methanesulfonyl fluoride (MSF), was discovered to have low toxicity, central nervous system (CNS) selectivity, and a long therapeutic duration. The purpose of this research was to determine if MSF (1.5 mg/kg) would be effective in reducing or blocking amnesia induced by various doses of scopolamine (0.2, 0.6, and 2.0 mg/kg). One hundred and twenty-two female Sprague-Dawley albino rats were trained and retention tested in a Y-maze brightness discrimination task. MSF was highly effective in reducing scopolamine-induced amnesia.

Amnesia↗
PubMed1983

Amnesia, pain experience, and patient satisfaction after sedation with intravenous diazepam.

Recovery time, the effect of sedation or amnesia on postoperative pain, and patients' opinions of the sedation were studied. Forty operations were performed on 20 patients. Each patient had four impacted third molars removed in two sessions, one in which a new emulsion form of diazepam (Diazemuls) was used, and one in which no sedation was used. The recovery from sedation was found to be very individual and not related to the dose administered, as assessed by a simple, easy-to-use method. There was no difference in postoperative pain between the sedated and unsedated groups, and we found no correlation between postoperative pain and amnesia. Eighty-five per cent of the patients preferred sedation during surgery, even though none of them had a preoperative indication for sedation.

Adolescent↗
PubMed1988

Preserved learning of novel information in amnesia: evidence for multiple memory systems.

Four of five patients with marked global amnesia, and others with new learning impairments, showed normal processing facilitation for novel stimuli (nonwords) and/or for familiar stimuli (words) on a word/nonword (lexical) decision task. The data are interpreted as a reflection of the learning capabilities of in-line neural processing stages with multiple, distinct, informational codes. These in-line learning processes are separate from the recognition/recall memory impaired by amygdalohippocampal/dosomedial thalamic damage, but probably supplement such memory in some tasks in normal individuals. Preserved learning of novel information seems incompatible with explanations of spared learning in amnesia that are based on the episodic/semantic or memory/habit distinctions, but is consistent with the procedural/declarative hypothesis.

Adolescent↗