Retrograde amnesia: electroconvulsive shock effects after termination of rapid eye movement sleep deprivation

Mice that were deprived of rapid eye movement sleep for 2 days immediately after one-trial training in an inhibitory avoidance task and were given an electroconvulsive shock after deprivation displayed retrograde amnesia on a retention test given 24 hours later. Electroconvulsive shock produced no amnesia in comparable groups of animals that were not deprived of rapid eye movement sleep.     

Recovery from retrograde amnesia: a learning process

Retrograde amnesia was produced in rats by electroconvulsive shock. Memory recovered if the animals were given repeated test trials. Memory did not recover if steps were taken to reduce the conditioning properties of the test trials; the manipulations included eliminating the response, altering the apparatus cues, or extinguishing conditioned "fear" by confining animals to the apparatus during the first test trial.     

Effects of Electroshock on Memory: Amnesia without Convulsions

Mice received a single training trial on an inhibitory avoidance task and a retention trial 24 hours later. Electroshock stimulation, administered 25 seconds after the training trial, produced amnesia even if the convulsion was prevented by ether anesthesia. The amnesia produced by such shock is apparently due to the electric current and not to the convulsion.     

Electroconvulsive shock effects on a reactivated memory trace: further examination

Rats showed amnesia for conditioned fear training if given an electroconvulsive shock immediately after training. Retention was unimpaired, however, when the electroconvulsive shock treatment was given 1 day after training immediately after the presentation of the stimulus used in the fear conditioning training. These results support the view that electroconvulsive shock disrupts memory trace consolidation but does not disrupt a recently reactivated memory trace.     

Recovery of memory after amnesia induced by electroconvulsive shock

Electroconvulsive shock given to rats immediately after one-trial avoidance learning produced a significant amnesic effect 24 hours later; this amnesia had largely disappeared in further retention tests 48 and 72 hours after treatment. This result puts in question a basic assumption implicit in most memory consolidation studies that such amnesic effects will be permanent.     

Long temporal gradient of retrograde amnesia for a well-discriminated stimulus

This experiment tested the general validity of recent findings that retrograde amnesia can be produced by electroconvulsive shock only if the shock is administered within 10 to 30 seconds after the learning trial. Precautions were taken to avoid confusion of other shock effects with retrograde amnesia. A temporal gradient of elec- troconvulsive shock-produced retrograde amnesia, extending up to at least 1 hour, for a well-discriminated stimulus, was demonstrated in mice in a one-trial learning passive avoidance situation.     

Permanence of retrograde amnesia produced by electroconvulsive shock

The permanence of retrograde amnesia produced for a single training trial by a single electroconvulsive shock was studied. No recovery from amnesia was found with either single or repeated retention tests. Amnesic effects were found to be permanent with retention intervals as long as 1 month.     

Retrograde amnesia gradients: effects of direct cortical stimulation

Electrical stimulation was delivered bilaterally to either the anterior or posterior cortex in rats from 0.1 second to 4 hours after a single training trial on an inhibitory avoidance task. As indicated by a retention test given 24 hours later, the length of the retrograde amnesia gradients ranged from 5 seconds to 240 minutes, depending on the brain region stimulated and the intensity of the stimulating current. The stimulation intensity that was threshold for amnesia varied directly with the length of the interval between training and treatment.     

Amnesia: a function of the temporal relation of footshock to electroconvulsive shock

When rats received a brief footshock upon stepping off an elevated platform, and an electroconvulsive shock 30 seconds or 6 hours afterward, amnesia was not observed 24 hours later. If a second footshock (noncontingent) was delivered 0.5 second before the electroconvulsive shock, amnesia was observed. The amnesia was temporary if conditioning was strong and permanent if conditioning was weak.     

Retrograde Amnesia from Conditioned Competing Responses

If electroconvulsive shock is given immediately after a learning trial, retrograde amnesia for that response occurs. The usual interpretation of such amnesia states that a neural engram, after a learning trial, requires a certain amount of time to consolidate, and electroconvulsive shock interferes with this consolidation, producing amnesia. Four studies are summarized which indicate that convulsive shock serves as an unconditioned stimulus producing a convulsive response, that takes precedence over other behavior, and part of which becomes conditioned to stimuli in the learning situation. The convulsive response competes with, and replaces, the previous response, resulting in the appearance of amnesia.     

Retrograde amnesia and the "reminder effect": an alternative interpretation

Recent findings suggest that amnesic agents block the retrieval of stored information. "Reminder" treatments, such as noncontingent punishments given after the production of amnesia for avoidance learning, improve the later retention performance of an animal. The data reported suggest that noncontingent treatments provide an additional learning experience which adds to the retention performance of partially amnesic or poorly trained animals.     

Memory traces: experimental separation by cycloheximide and electroconvulsive shock

Mice given cycloheximide or saline were trained with a single trial. Electroconvulsive shock was administered to both groups at various times after training. Cycloheximide led to memory that decayed with time. Cycloheximide plus electroconvulsive shock produced complete amnesia at times when neither treatment alone produced amnesia. Only two types of processes appear to support memory storage in our study.     

Retrograde amnesia produced by electroconvulsive shock after reactivation of a consolidated memory trace

Rats had a memory loss of a fear response when they received an electroconvulsive shock 24 hours after the fear-conditioning trial and preceded by a brief presentation of the conditioned stimulus. No such loss occurred when the conditioned stimulus was not presented. The memory loss in animals given electroconvulsive shock 24 hours after conditioning was, furthermore, as great as that displayed in animals given electroconvulsive shock immediately after conditioning. This result throws doubt on the assertion that electroconvulsive shock exerts a selective amnesic effect on recently acquired memories and thus that electroconvulsive shock produces amnesia solely through interference with memory trace consolidation.     

Memory: modification of anisomycin-induced amnesia by stimulants and depressants

Mice were trained in a passive (foot shock)avoidance task. When administered after training, the stimulants caffeine or nicotine blocked amnesia for the task that had been produced by injections of the protein synthesis inhibitor anisomycin given prior to training. With foot shock at a higher intensity, anisomycin did not produce amnesia by itself, but the administration of the depressants chloral hydrate or sodium phenobarbital after training did cause amnesia. Stimulants and depressants did not have an appreciable influence on the overall degree of protein synthesis inhibition produced by anisomycin. The results support the hypothesis that arousal after training is an important factor in the conversion of short-term to long-term memory.     

Retrograde amnesia produced by intraperitoneal injection of physostigmine

Intraperitoneal injection of physostigmine in rats produced a retrograde amnesia of a trained task of escaping shock. This amnesic effect was a U-shaped function of the length of the interval between initial training and injection. In all cases, retraining Occurred 30 minutes after injection. A substantial effect was produced by physostigmine if its application was made 30 minutes after training; there was no effect if application and tests were made 1, 2, or 3 days after the original training. When the substance was injected and the rats were retrained 5, 7, or 14 days after the original training, a substantial effect again appeared. These results are similar to those reported in experiments in which another anticholinesterase, diisopropyl fluorophosphate, was applied intracerebrally. The data demonstrate a similar pattern of change of the amnesia with time, and they substantiate the view that neither the place of application nor the brain lesions caused the reported amnesia.     

Retrograde amnesia: production of skseletal but not cardiac response gradient by electroconvulsive shock

Rats given a single electroconvulsive shock immediately after but not 60 seconds after an aversive conditioning trial exhibited behavioral retention deficits 24 hours later in a one-trial passive avoidance task. In contrast to these differential performance deficits, similar heart-rate changes, indicative of fear retention, were seen in punished animals irrespective of the time of delivery of the shock. These data suggest retention of a generalized fear to the training experience that was not revealed by the behavioral measure. The potential usefulness of concomitant behavioral and physiological response assessment in consolidation research is discussed.     

Amnesia produced by spreading depression and ECS: evidence for time-dependent memory trace localization

Rats were given electroconvulsive shock and bilateral cortical spreading depression, either alone or in combination, at various times after a single passive avoidance training trial. Assessment of retention deficits, 24 hours after training, revealed a U-shaped amnesic function for cortical spreading depression as compared with the short linear function consistently obtained with electroconvulsive shock in this situation. Induction of cortical spreading depression immediately after training resulted in an extension of the amnesic gradient produced by electroconvulsive shock, presumably by disruption of the subcortically confined memory trace. In addition to indicating a stibcortical locus of action for the amnesic effects of electroconvulsive shock, these results are interpreted as favoring a hypothesis of time-dependent memory trace localization in short-term memory processing, which involves an initial subcortical localization of the trace followed by a phase involving either direct or indlirect cortical participation in a mulltistage memory fixation process.     

Anticholinesterase-induced amnesia and its temporal aspects

Injection of the anticholinesterase drug diisopropyl fluorophosphate into the hippocampi of rats, 30 minutes after escape learning, produces partial amnesia with full recovery 5 days after injection. No such amnesia is produced if the injection takes place 3 days after learning. However, with injections 5 days after learning there is again an effect, and at 14 days amnesia is complete though no normal forgetting occurs within this period.     

Amnesic effects of small bilateral brain puncture in the mouse

A small acute brain puncture produced retrograde amnesia in a passive avoidance learning situation in mice. If injury to the hippocampus was inflicted either immediately, 1 hour after the learning, or 1 hour before the learning, the animals showed a retention deficit; the degree of this deficit was related to the time interval. No effect of this injury was observed on retest performance when the animals were treated as long as 6 hours before or after the learning trial.     

Retrieval failure induced by electroconvulsive shock: reversal with dissimilar training and recovery agents

Amnesia was obtained following electroconvulsive shock in rats trained at one-trial passive avoidance of immersion in ice water. Avoidance behavior was restored when noncontingent foot shock was administered outside the training apparatus. The qualitative differences between ice water and foot shock demonstrate that the agent inducing recovery of memory need not be physically similar to the reinforcer used during training. These findings are interpreted as supporting a retrieval failure view of experimental amnesia.