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.     

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.     

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.     

Deficits in passive avoidance and fear conditioning in mice with septal lesions

By means of a simple activity measure, mice with lesions of the septal forebrain were tested for passive avoidance (response inhibition) and fear conditioning. In two separate experiments animals with septal lesions showed little or no conditioning, as evidenced by lack of suppression of activity during and following activitycontingent foot shock. Results support and extend thehypothesis that these deficits in passive avoidance derive from the removal of normal inhibitory influences mediated by the septal area.     

Amnesia produced by electroconvulsive shock or cycloheximide: conditions for recovery

Retrograde amnesia for a passive avoidance response was produced in rats by electroconvulsive shock and in mice by cycloheximide, an inhibitor of protein synthesis. One day after training the memory could be restored if a "reminder" of the original foot shock was given after the retention test on which the amnesia was demonstrated. Memory did not return if the reminder was given without the prior retention test or if the reminder and the test were separated by 23 hours.     

Theta rhythm: a temporal correlate of memory storage processes in the rat

We examined the amount of theta rhythm (4 to 9 hertz) in cortical electroencephalograms of rats for 30 minutes after training in one-trial tasks. Some animals received electroconvulsive shock after training. The amount of theta in the electroencephalogram after training was positively correlated with the degree of subsequent retention of a footshock, whether animals had received electroconvulsive shock or not.     

Paradoxical fear-increasing effects of tranquilizers: evidence of repression of memory in the rat

Conditioned suppression of feeding, an index of fear, was increased rather than decreased by the administration of benzodiazepine tranquilizers or amobarbital. The drug-induced increase in conditioned fear varied directly with the intensity of the shock used in fear conditioning. The drugs had no fear-increasing effect in unshocked controls or in rats made amnesic by electroconvulsive shock given immediately after fear conditioning. These observations in animals are reminiscent of clinical reports that intraveneous amobarbital facilitates the recall of repressed traumatic experiences. The retrieval of painful memories may be inhibited or repressed in animals as well as in humans. In both cases, tranquilizers may counteract repression by disinhibition of the act of retrieval.     

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.     

Phenylketonuria in rats: reversibility of behavorial deficit

Phenylketonuria was induced in hooded rats by the conventional procedure of feeding excessive quantities of L-phenylalanine after weaning. Although this procedure reliably induced large, dose-dependent deficits in performance on a water maze, the behavioral deficits were completely eliminated after cessation of phenylalanine loading. These results cast doubt on the assumption that this animal preparation adequately simulates the irreversible intellectual impairments found in the child with late-detected phenylketonuria.     

Memory disruption by electrical stimulation of substantia nigra, pars compacta

Electrical stimulation of the substantia nigra, pars compacta, of albino rats while they were learning a simple foot shock task of withdrawal and response suppression disrupted retention of that task 24 hours after original learning. Stimulation in the reticular zone of the substantia nigra was without effect on retention performance. Stimulation through electrodes in the medial lemniscus, red nucleus, or brainstem regions surrounding the substantia nigra, pars compacta, was also ineffective. Original learning performance, measured as time to criterion, was unimpaired by the stimulation. Posttrial stimulation in the substantia nigra, pars compacta, but not in adjacent structures, also disrupted retention performance.     

Interpeduncular nucleus and avoidance conditioning in the rat

Rats trained to make a jumping response to the onset of a visual stimulus lost the habit after damage to the interpeduncular nucleus of the midbrain. It was noted, however, that the majority of the operated animals showed perfect retention of the "fear" response to the conditioned stimulus.     

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.     

Puromycin and retention in the goldfish

A first experiment compared the behavior of goldfish injected with puromycin immediately after each of a weekly series of brief discriminative training sessions in the shuttlebox to that of appropriate controls. Discrimination was not prevented, nor was escape from shock impaired, but probability of response to the conditioned stimuli, both positive and negative, was reduced substantially. These results suggest that puromycin interferes with the consolidation of conditioned fear. The null outcome of a second experiment, in which all training was given in a single long session instead of a series of short sessions, suggests (contrary to recent indications) that consolidation begins in the training session. The conditioned-fear hypothesis is supported by the results of a third experiment in which the animals were shocked upon entering a goalbox to which they had previously learned to swim for food; animals injected with puromycin, immediately after the shock, entered the goalbox more readily 1 week later than did appropriate controls.     

Epinephrine enables Pavlovian fear conditioning under anesthesia

Rats under Pavlovian defensive conditioning (noise paired with shock) while under general anesthesia. Peripheral administration of epinephrine (0.01 to 1.0 milligram per kilogram of body weight) during training resulted in the acquisition of conditioned fear, as shown 10 days later by conditioned suppression of water drinking. Analysis of heart rate and measurement of reflexes during training indicated that epinephrine did not lighten the state of anesthesia. These results indicate that epinephrine enables the learning of conditioned fear in the anesthetized brain.     

Calcium-permeable AMPA receptor dynamics mediate fear memory erasure

Traumatic fear memories can be inhibited by behavioral therapy for humans, or by extinction training in rodent models, but are prone to recur. Under some conditions, however, these treatments generate a permanent effect on behavior, which suggests that emotional memory erasure has occurred. The neural basis for such disparate outcomes is unknown. We found that a central component of extinction-induced erasure is the synaptic removal of calcium-permeable α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptors (AMPARs) in the lateral amygdala. A transient up-regulation of this form of plasticity, which involves phosphorylation of the glutamate receptor 1 subunit of the AMPA receptor, defines a temporal window in which fear memory can be degraded by behavioral experience. These results reveal a molecular mechanism for fear erasure and the relative instability of recent memory.     

Oxytocin selectively gates fear responses through distinct outputs from the central amygdala

Central amygdala (CeA) projections to hypothalamic and brain stem nuclei regulate the behavioral and physiological expression of fear, but it is unknown whether these different aspects of the fear response can be separately regulated by the CeA. We combined fluorescent retrograde tracing of CeA projections to nuclei that modulate fear-related freezing or cardiovascular responses with in vitro electrophysiological recordings and with in vivo monitoring of related behavioral and physiological parameters. CeA projections emerged from separate neuronal populations with different electrophysiological characteristics and different response properties to oxytocin. In vivo, oxytocin decreased freezing responses in fear-conditioned rats without affecting the cardiovascular response. Thus, neuropeptidergic signaling can modulate the CeA outputs through separate neuronal circuits and thereby individually steer the various aspects of the fear response.     

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.     

Ether-induced retrograde amnesia for one-trial conditioning in mice

Mice were tested in a situation permitting them to step readily from a small, restrictive platform to a larger one. Conditioned avoidance was established by a single training trial when animals received a shock by stepping from one platform to another. At various intervals after the single punishing shock, subjects were anesthetized with diethyl ether. Interference with retention, tested 1 day later, was shown for intervals up to 24 minutes, at which time ether no longer appeared to influence the subsequent response.     

Hypolinimetic oxygen deficits: their prediction and interpretation

Rates of hypolimnetic oxygen depletion can be predictedfrom a knowledge of a lake's phosphorus retention, the average hypolimnetic temperature, and the mean thickness of the hypolimnion. Areal oxygen deficits cannot be used to index lake trophic status because areal calculations do not eliminate the influence of hypo-limnetic morphometry.