Selective recovery from retrograde amnesia produced by hippocampal spreading depression

Injections of potassium chloride into the hippocampus after learning produce temporary disruption of neural activity and retrograde amnesia. Recovery from the amnesia is selective-rats recover from amnesia of events that occurred24 hours before injection but do not recover from amnesia of events that occurred 10 seconds before injection.     

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 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.     

Retrograde amnesia in free recall

Supervention of high-priority events in a series of events constituting a free-recall task interferes with postexposure processing of mnemonic information about immediately preceding events, with the result that recall of these preceding events is impaired. Recall of immediately following events is not affected. This retrograde interference is time dependent.     

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.     

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: effects of handling and microwave radiation

Rats that were irradiated with microwaves immediately after the training trial in a one-trial shock-avoidance learning task retained the conditioned avoidance response 24 hours later. However, rats that were handled a few minutes each day for 3 days before the experiment did not retain the response, although they were capable of learning in a later test.     

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.     

Drinking and eating elicited by cortical spreading depression

Single waves of unilateral and bilateral cortical spreading depression were administered to rats by electrophoretic injection of potassium ions into the occipital cortices. Aggressive and stereotyped eating, drinking, and exploratory behavior were elicited by unilateral and bilateral spreading depression. Onset of the elicited behaviors varied among rats from 4 to 8 minutes after injection of the ions. Direct activation of, or rebound from, inhibition of subcortical motivational mechanisms may be responsible for the effects.     

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.     

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.     

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.     

Amino acid incorporation into rat brain proteins during spreading cortical depression

Unilateral spreading cortical depression was elicited by applying potassium chloride solutions to the dura of conscious, freely moving rats. Incorporation of (3)H-leucine into soluble cortical proteins was decreased in the depressed hemisphere relative to the control side, while soluble brainstem proteins from both sides had the same specific activity. Various subfractions of soluble cortical proteins were affected to equal degrees.     

Lack of coincidence between neural and behavioral manifestations of cortical spreading depression

The presence of cortical spreading depression is typically inferred from the presence of hypesthesia. The electrocorticogram and slow-potential change were recorded during cortical spreading depression and it was found that hypesthesia remained long after the cortex recovered from neural depression. Hypesthesia, therefore, is an unreliable indicant of cortical spreading depression; if cortical spreading depression is used as a research tool, neural activity must be monitored. These data offer a special problem for memory transfer studies.     

Muscarinic depression of long-term potentiation in CA3 hippocampal neurons

Behavioral studies have suggested that muscarinic cholinergic systems have an important role in learning and memory. A muscarinic cholinergic agonist is now shown to affect synaptic plasticity in the CA3 region of the hippocampal slice. Long-term potentiation (LTP) of the mossy fiber-CA3 synapse was blocked by muscarine. Low concentrations of muscarine (1 micromolar) had little effect on low-frequency (0.2 hertz) synaptic stimulation but did significantly reduce the magnitude and probability of induction of LTP. Experiments under voltage clamp showed that muscarine blocked the increase in excitatory synaptic conductance normally associated with LTP at this synapse. These results suggest a possible role for cholinergic systems in synaptic plasticity.     

Role for rapid dendritic protein synthesis in hippocampal mGluR-dependent long-term depression

A hippocampal pyramidal neuron receives more than 10(4) excitatory glutamatergic synapses. Many of these synapses contain the molecular machinery for messenger RNA translation, suggesting that the protein complement (and thus function) of each synapse can be regulated on the basis of activity. Here, local postsynaptic protein synthesis, triggered by synaptic activation of metabotropic glutamate receptors, was found to modify synaptic transmission within minutes.     

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.     

A sea-floor spreading event captured by seismometers

Two-thirds of Earth's surface is formed at mid-ocean ridges, yet sea-floor spreading events are poorly understood because they occur far beneath the ocean surface. At 9 degrees 50'N on the East Pacific Rise, ocean-bottom seismometers recently recorded the microearthquake character of a mid-ocean ridge eruption, including precursory activity. A gradual ramp-up in activity rates since seismic monitoring began at this site in October 2003 suggests that eruptions may be forecast in the fast-spreading environment. The pattern culminates in an intense but brief (approximately 6-hour) inferred diking event on 22 January 2006, followed by rapid tapering to markedly decreased levels of seismicity.