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Disturbances were studied of the motor defensive conditioned reflexes in rats radiated in a dose of 100 Gy at different stages of formation and stabilization of temporary connection. In comparison with consolidated (automatized) conditioned reflexes of active avoidance, early stages of formation and stabilization of the temporary connection are characterized by a relatively low resistance against extreme factors and by deepest disturbances of reproduction in radiated animals. The most probable mechanisms of these disturbances are connected with pathological changes of the nervous processes balance towards an increase of excitability and weakening of internal inhibition. Yet a direct radiation influence on the mechanisms of temporary connection reproduction at the second stage of its consolidation cannot be excluded. The role is shown of the emotional reactivity in the above-described processes.

The author, by giving an outline of one particular case as well as a survey of the relevant literature on transient global amnesia, describes the characteristic clinical picture that is characterized by a sudden loss of what is known as the short-time memory, which usually lasts for several hours, as well as by retrograde amnesia which sometimes dates back to many years. The condition gradually fades away within a few hours or during a night's sleep, and what remains is lack or loss of memory for the episodic period or sometimes retrograde amnesia. Relapses were not observed in the majority of patients. The disease usually develops in people in their sixth to eighth decades of life. The cause of the disease is not yet fully understood. Accordingly, it is justified to use such terms as autochthonous or cryptogenic amnestic episodes. The disease is also discussed from a differential diagnosis point of view.

Disrupting circadian organization by exposing rats to a shifted illumination schedule after training for passive avoidance and shuttle box avoidance behavior resulted in retrograde amnesia as evidenced by impaired performance during retention and extinction testing respectively. A single treatment with either the ACTH-(4-9) analog ORG 2766 or desglycinamide9-(Arg8)-vasopressin (DGAVP) 1 hour prior to the retention of passive avoidance or extinction of shuttle box avoidance behavior restored the behavioral impairment. It is suggested that these peptides may be useful to relieve memory deficits induced by disturbances in circadian organization.

Restoration of memory by pretest reminder treatments following ECS-induced amnesia in principle could be mediated by nonassociative arousal and/or reactivation of information by the reminder stimuli. In the present research, arousal value of the reminder treatment was largely a function of the novelty of the context in which the reminder cues occurred. After producing ECS-induced amnesia in rats for a signaled passive avoidance task, presentation of the signal outside of the training and test context proved to be an effective reminder cue. However, prereminder familiarization with the reminder location, which was sufficient to reduce exploratory behavior suggestive of a decrease in the arousal value of the context, did not influence recovery from amnesia. These data indicate that reminder treatments are capable of reversing experimental amnesia by initiating further processing of previously acquired information even when the treatment does not produce appreciable arousal.

The time course of antirecall effect and grades of sedation after the oral administration of diazepam and lorazepam were determined in 120 patients. Three standard doses of each drug were employed. Grades of sedation following oral diazepam were dose related, with a latency of 30-60 min and duration of 120-150 min. All three doses of lorazepam produced significantly more sedation with a similar latency (30-60 min) but longer duration (more than 240 min). Peak frequencies of the antirecall effects of diazepam 10, 15, and 20 mg were 5, 20, and 30 per cent, respectively. The duration was about two hours. Peak frequencies of the antirecall effect after lorazepam 2, 3, and 4 mg were 30, 45, and 72 per cent, respectively. Latency of peak action was about 60-90 min for all the doses, but the duration, especially with 3 and 4 mg doses, was long (4 h).

Aging mice showed a retrograde amnesia for passive avoidance behavior when a single electroconvulsive shock (ECS) was given at post-training intervals up to 1 h, whereas adult mice showed no significant amnesia when ECS was given 10 min or more after training. Catecholamines (norepinephrine and dopamine), but not serotonin (5-HT) changed with aging in the several brain regions, but only 5-HT was significantly changed (elevated) by ECS. Protein synthesis was significantly inhibited by ECS, notably in limbic structures. The increased susceptibility of aging mice to the amnesic effect of ECS could be related to aging-related changes in the rate of memory consolidation or to the duration of neural chemical changes that disrupt processes such as consolidation, storage, and/or retrieval of the memory trace.

Recent studies of animals with complex nervous systems, including humans and other primates, have improved our understanding of how the brain accomplishes learning and memory. Major themes of recent work include the locus of memory storage, the taxonomy of memory, the distinction between declarative and procedural knowledge, and the question of how memory changes with time, that is, the concepts of forgetting and consolidation. An important recent advance is the development of an animal model of human amnesia in the monkey. The animal model, together with newly available neuropathological information from a well-studied human patient, has permitted the identification of brain structures and connections involved in memory functions.

Formal neuropsychological evaluation in patient with transient global amnesia (TGA) associated with migraine was performed 6 days and 17 months after the episode. Verbal learning difficulties and verbal IQ deficit were observed in line with the neuropsychological profile seen in the follow-up of TGA. A common origin for the TGA-Migraine episode and isolated TGA is discussed.

Rats were conditioned to fear a tone paired with shock to the feet. Retention tests 4 days later showed that consolidation had occurred. Other animals were not tested for retention at 4 days, but the tone was presented in order to reactivate their memories of the conditioning. An amnesia gradient was generated by low-intensity electrical stimulation of the amygdaloid complex at different intervals after the tone, but stimulation was without effect either when given to rats not previously conditioned or when given to conditioned rats without preceding memory reactivation. Thus, stimulation of the amygdaloid complex can can affect memory retrieval. Moreover, the data call into question the assumption that an amnesia gradient indicates that the memory consolidation process has been modified.

In the present study the effects of intracerebroventricularly [icv] administered somatostatin [linear and cyclic], somatostatin3-6, somatostatin7-10 and des AA1,2,4,5,12,13 [D-Trp8] somatostatin [ODT8-SS] were investigated on electroconvulsive shock [ECS]-induced retrograde amnesia in rats. The ECS significantly decreased the foot shock-induced avoidance latency, and thus caused retrograde amnesia. Somatostatin [linear and cyclic] in a dose of 0.6 nM had no action on the ECS-induced retrograde amnesia, while in doses of 3 nM and [cyclic only] 6 nM it significantly prevented it. Somatostatin3-6, somatostatin7-10 and ODT8-SS in doses of 0.6, 3 and 6 nM had no effect on the ECS-induced amnesia. These results indicate that the whole sequence of the original somatostatin molecule is needed to block the ECS-caused retrograde amnesia.

Naive and pretrained rats were trained in two active avoidance paradigms using a pole-climbing box and in a single-trial passive avoidance task using a T-maze. They were then subjected to amnestic treatments with electroshock, leptazol, pentobarbitone, or ether anesthesia. Single retention tests were given at 20-24, 44-48, or 68-96 h posttreatment. Electroshock and leptazol seizures produced retrograde amnesia in all three paradigms, provided that seizures were maximal and retention was tested before 48 h. Prior treatment with anticonvulsant drugs prevented amnesia. Ether and pentobarbitone anesthesia failed to produce amnesia in all three tasks. A trend of recovery from amnesia was observed in the electroshock and leptazol groups when tested for retention 48-96 h posttreatment. On the other hand, the non-amnesic control, pentobarbitone, and ether groups showed signs of forgetting at these longer intervals. Consolidation failure and/or retrieval block was surmised to be the cause of amnesia; recovery was the possible result of removing the block.

In this study, the possible role of overt convulsions following pentylenetetrazol (PTZ) in retrograde amnesia was investigated. Following a single passive avoidance conditioning, when overt convulsions were blocked with sodium pentobarbital (Nem), the amnesic effect of pentylenetetrazol was also blocked. Subconvulsive doses of the drug did not produce amnesia. Animals that received a typically convulsive dose of the drug but failed to convulse were not amnesic; only animals with overt convulsions were different from saline controls. The data suggest that overt convulsions may be necessary for the development of pentylenetetrazol-induced retrograde amnesia.

The problem was studied whether an initial preference of one limb exists in rats connected with interhemispheric asymmetry or it appears during the procedure of testing (the first successful movement of one limb becomes consolidated). The work consisted in obtaining experimental retrograde amnesia after preliminary determination of the preferred limb and in the following testing of the preference after a definite time interval. In this case the trace of preceding learning must not influence the following choice of the limb. It is shown that the preference in rats is not a result of accidental learning in the experiment but initially exists before testing procedure. Retaining of memory trace for a long time (2-4 weeks) is also shown even after a very short learning (one-three successful movements).

Relative role was studied of the "initial" preference (caused by animals individual properties) and learning in real preference of one limb in rats. After a short-time learning to get food from a narrow horizontal pipe only by the left paw a retrograde amnesia was evoked in rats. At preference determination after three weeks, in conditions which allowed to get food by any paw, in the group of animals without amnesia the number of the left-handed rats was 5.7 times more than of the right-handed ones. In the group of animals with amnesia the numbers of the left-handed, right-handed and ambidextrous were approximately equal. Correlation was revealed between the speed of learning to get food by the left paw and the number of attempts to use the right paw. It has been shown that the initial preference may be stably changed even by a short-time learning (3 food seizures). By the degree of manifestation of the initial preference the rats form a continuum with a gradual transition from pronounced right-handed animals to pronounced left-handed ones. The weaker is the initial preference, the greater the role of learning in the real preference of one of the paws.

The effects of several doses of intracerebroventricularly injected cholecystokinin octapeptide sulfate ester (CCK-8-SE) and nonsulfated scholecystokinin octapeptide (CCK-8-NS) were studied on electroconvulsive shock (ECS)-induced retrograde amnesia, as measured in a one-trial step-through passive avoidance paradigm. Both CCK-8-SE and CCK-8-NS were able to attenuate amnesia slightly when they were injected into rats 10 min prior to ECS treatment, possibly by reducing the severity of the ECS-induced seizures. Of the treatments carried out immediately after ECS, only the 0.8 pmole dose of CCK-8-NS could significantly restore retrograde amnesia. After treatment 20 min prior to testing 24-hr retention, no effect of the peptides was observed. The lack of a dose-dependency and of any effect on retrieval raises the possibility that the CCK octapeptides influence memory processes by an indirect mechanism.

Post-trial injections of norepinephrine (NE) or cycloheximide (CHX) into the amygdala produces a long-term retention deficity (amnesia) for a 1-trial footshock experience in rats. concomitant post-trial injections of the adrenergic antagonist, propranolol, prevents NE-, but not CHX-induced amnesia. These results indicate separate mechanisms of action for amnesia produced by intracranial CHX and NE injections.

Although there have been several reports that preweanling rats and mice are relatively resistant to experimentally induced retrograde amnesia, there is virtually no information concerning susceptibility to anterograde amnesia in subjects of this age. Therefore, in the present experiment, 23-day-old rats received hypothermia either prior to, or immediately after, punishment training in an attempt to induce anterograde and retrograde amnesia, respectively. When tested 24 hr later, only those subjects given hypothermia prior to training exhibited any loss of retention. Thus these results confirmed previous evidence of resistance to retrograde amnesia in preweanling rats and further demonstrated that substantial anterograde amnesia could be obtained in these subjects. Performance of subjects tested after a 5-min retention interval revealed that the poor retention performance in subjects cooled prior to training and tested 24 hr later was not due to a learning deficit. These results are also discussed with respect to the issue of the independence of anterograde and retrograde amnesia.

To analyze disorders of memory functions, observations were made in healthy test subjects after administration of psychotropic drugs and anesthetics. In isolated cases amnesic episodes were recorded and in 8 of the subjects accurate measurements of the retrograde amnesia after propanidid anesthesia were made. The observations provided arguments for the delimitation of the immediate memory (ultra-short-term memory, one minute memory) from short-term memory and long-term memory of the conventional terminology. As a result of our investigations we came to the thesis that the transformation of the non-specific biochemical and electrophysiological processes underlying the immediate memory into the specific processes underlying the short-term memory is more susceptible to disturbances than that of reproduction and the processes serving for perception. With regard to forensic assessment, it is significant that behaviour foreign to the personality could not be observed in amnesic episodes.

Transient global amnesia (TGA) is an unusual form of the amnestic syndrome, clinically characterized by profound disturbance of short-term memory with preservation of immediate recall and long-term memory. Spontaneous recovery is the rule and is usually complete within several hours. The etiology of TGA is not clear. It is considered to be caused by transient ischemia confined to the medial temporal lobe, an area supplied by branches of the vertebrobasilar system. Basilar artery migraine is a well-known syndrome, first described by Bickerstaff. Besides pulsating headache, the dominant symptoms are vertigo, ataxic gait, tinnitus, dysarthria, paraeshesia in the hands, homonymous hemianopsia and sometimes drop-attacks. These symptoms are associated with vertebrobasilar system dysfunction. In this paper, three migraine patients, suffering from one episode of TGA, were reported. All patients were women. Case 1 was a 48-year-old woman with a history of common migraine. Case 2 was a 48-year-old woman with a history of classic migraine. Case 3 was a 59-year-old woman with a common migraine. Family history of migraine exists in case 1 and case 3. Their migrainous attacks began in their twenties and thirties. They suddenly suffered migraine with the symptoms of vertebrobasilar dysfunction. These symptoms are ataxic gait (Case 1, 2, 3), dysarthria (Case 1, 2), vertigo (Case 1, 3) and homonymous hemianopsia (Case 1, 3). Simultaneously three patients had TGA. Duration of retrograde amnesia were about twenty-four hours (Case 1), about thirty minutes (Case 2) and about three hours (Case 3).(ABSTRACT TRUNCATED AT 250 WORDS)

Old memory, when reactivated by cue exposure, was disrupted by mild or deep hypothermia treatments. New memory was impaired only by deep cooling. Moreover, old but not new learning showed spontaneous recovery. Old reactivated memory may be qualitatively different from newly acquired memory.