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Query: UMLS:C0598853 (forgetting)
 3,232 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

These observations indicate that the long-lasting trace of an experience is not completely fixed, consolidated, or coded at the time of the experience. Consolidation requires time, and under at least some circumstances the processes of consolidation appear to be susceptible to a variety of influences- both facilitating and impairing- several hours after the experience. There must be, it seems, more than one kind of memory trace process (31). If permanent memory traces consolidate slowly over time, then other processes must provide a temporary basis for memory while consolidation is occurring. The evidence clearly indicates that trial-to-trial improvement, or learning, in animals cannot be based completely on permanent memory storage. Amnesia can be produced by electroshock and drugs even if the animals are given the treatment long after they have demonstrated "learning" of the task. Of particular interest is the finding that retention of the inhibitory avoidance response increases with time. In a sense this should be expected, for it has long been known (and ignored) that, within limits, learning is facilitated by increasing the interval between repeated trials (7, 30). Our result may be the simplest case of such an effect. Since the improvement in retention with time seemed not to be due solely to consolidation (as indicated by electroshock effects), it would seem that the "distribution of practice" effect, as it is typically designated, may be due in part to a time-dependent temporary memory storage process. In our work with animals we have found no analog of human immediate memory such as that required for repeating digits (or finishing sentences). Animals tested immediately on the task described above after a trial typically showed no evidence of memory. It could be that the poor performance is due to excessive fright, but the "distribution of practice effect" is also typically observed in learning experiments in which food reward is used rather than shock avoidance. Since the retention tasks require the animals to change their behavior in some way, it could well be that the growth of retention over the first few minutes after a trial is due to time dependent processes involved in the organization of processes necessary for changing behavior, in addition to those involved in temporary storage and retrieval. It is worth pointing out that there is evidence of an analogous process in human memory (32). A complex picture of memory storage is emerging. There may be three memory trace systems: one for immediate memory (and not studied in our laboratory); one for short-term memory which develops within a few seconds or minutes and lasts for several hours; and one which consolidates slowly and is relatively permanent. The nature of the durability of the longterm memory trace (that is, the nature and basis of forgetting) is a separate but important issue. There is increasing evidence and speculation (20, 21, 33) that memory storage requires a "tritrace" system, and our findings are at least consistent with such a view. If there are, as seems possible, at least three kinds of traces involved in memory storage, how are they related? Is permanent memory produced by activity of temporary traces (31), or are the trace systems relatively independent? Although available findings do not provide an answer to this question, there does seem to be increasing evidence that the systems are independent. Acquisition can occur, as we have seen, without permanent consolidation, and both short-term and long-term memory increase with time. All this evidence suggests (but obviously does not prove) that each experience triggers activity in each memory system. Each repeated training trial may, according to this view, potentiate short-term processes underlying acquisition while simultaneously enhancing independent underlying long-term consolidation. Obviously, acceptance of these conclusions will require additional research. If this view is substantially correct, it seems clear that any search for the engram or the basis of memory is not going to be successful. Recognition of the possibility that several independent processes may be involved at different stages of memory may help to organize the search. A careful examination of the time course of retention and memory trace consolidation, as well as examination of the bases of the effects of memory-impairing and memory-facilitating treatments, may help to guide the search. It is clear that a complete theory of memory storage must eventually provide an understanding of time-dependent processes in memory. In 1930 Lashley wrote (2), "The facts of both psychology and neurology show a degree of plasticity, of organization, and of adaptation and behavior which is far beyond any present possibility of explanation." Although this conclusion is still valid, the current surge of interest in memory storage offers hope that this conclusion may soon need to be modified.
Science 1966 Sep 16
PMID:Time-dependent processes in memory storage. 591 68

In order to attempt to measure everyday forgetting experiences outside the laboratory, groups of undergraduates, healthy old people, and neuropathological patients with memory complaints were asked to use portable memory diaries. For a period of 7 days, they were immediately to write down every instance of noticing that they had forgotten anything. Types of forgetting, their frequency, and types of cues in the world that served as reminders that forgetting had occurred are discussed.
Cortex 1984 Sep
PMID:Everyday forgetting experiences: real-time investigations with implications for the study of memory management in brain-damaged patients. 648 12

Rats were trained on a succession of two-odor discriminations for a water reward in a modified radial maze. A different odor pair was used each day. After three or four pairs, rats would learn to choose the correct odor in only 3-5 trials. Animals were then subjected to electrolytic lesions in the lateral entorhinal cortex, which is innervated by the lateral olfactory tract, or in the dorsal entorhinal cortex, which is not a target of the olfactory system. Lesions of the first type did not interfere with performance, provided a short interval (30 sec to 2 min) was used between trials. However, the rats were severely impaired when trials were separated by 3-10 min. Dorsal lesions had no effect on olfactory discrimination irrespective of length of delay. In additional experiments, the rats were trained for 10 trials with short inter-trial intervals and then tested 1 hr later with the significance of the cues reversed. Animals with dorsal lesions continued to respond to the formerly correct odor while those with lateral entorhinal damage immediately reversed their response choices. These results provide evidence that lesions to the hippocampal system produce a rapid forgetting syndrome in rats comparable with that reported for humans with temporal lobe damage or dysfunction.
Proc Natl Acad Sci U S A 1984 Sep
PMID:Hippocampal denervation causes rapid forgetting of olfactory information in rats. 659 92

A staircase maze has been used to test the modification induced by a chronic administration of different doses of diazepam in the decay of the rat performance caused by an interruption of 20 days in the daily training. The possibility that behavioral interferences modify the diazepam effect has been examined by testing the rat in an open field or in a Y maze during the interruption of the training in the staircase maze. The diazepam effect on the rat behavior in the staircase maze increased linearly with the doses; an intercalated training in the open field increased the diazepam effect, while an intercalated training in a Y maze completely abolished the increase of forgetting caused by diazepam.
Life Sci 1983 Sep 26
PMID:Behavioral interferences modify the acceleration in memory decay caused by diazepam. 688 75

Discrimination learning, memory, and transfer capacity were assessed in representative samples of institutionalized retarded persons in order to provide information on trainability. The 56 subjects were selected from moderately, severely, and two levels of profoundly retarded adults. They learned and relearned three successive two-choice discrimination problems. Generally, the higher functioning subjects, defined by IQ and adaptive behavior learned more rapidly than did the lower functioning subjects. Forgetting was related to IQ/adaptive behavior level. Interproblem transfer was negligible at all levels of retardation, but ceiling effects may have obscured positive transfer in the higher functioning groups. Backward learning curves revealed large differences between lower and higher functioning persons in the presolution trials, but once learning began even profoundly retarded subjects solved these problems as rapidly as did the moderately retarded subjects. Ten of the 56 subjects failed to learn all three problems.
Am J Ment Defic 1982 Sep
PMID:Learning, memory, and transfer in profoundly, severely, and moderately mentally retarded persons. 712 31

The retention performance of young (3-6 months) and aged (24-26 months) Sprague-Dawley rats was evaluated on three separate experimental paradigms. The three paradigms were sequenced so that the first, spontaneous alternation, tested for retention performance of short-term memory; the second, step-down inhibitory (passive) avoidance, tested for long-term memory; while the third, a shock-motivated spatial reversal problem, tested for both short- and long-term memory. The results suggest that aged rats experience significantly more rapid forgetting in both short- and long-term memory systems.
Behav Neural Biol 1982 Sep
PMID:Rapid forgetting in aged rats. 716 30

In a series of 7 experiments we investigated the possibility that juvenile rats show long-term retention for aspects of early avoidance training and that these retained elements serve to reinforce relearning of the forgotten operants. Rats trained in active or passive avoidance at 23-25 days of age demonstrated the typical juvenile forgetting effect relative to adults after a 28-day interval. However, both juveniles and adults demonstrated marked reductions in locomotor activity prior to retraining which were specific to the apparatus and not dependent on the opportunity to perform an operant during initial training. Juvenile animals given a reminder exposure plus footshock 27 days after training, then single daily nonshock trials (Days 28-30), showed decreasing crossover latencies across days if trained in active avoidance and increasing latencies if trained in passive avoidance. This reappearance of task-appropriate crossover latencies was evident in previously trained juveniles only. Finally, young animals' demonstrated change in crossover latency is associated with subsequent superior acquisition performance, and this change depends upon the presentation of the test trials for its appearance. We suggest that the amelioration of "infantile amnesia asociated with the present procedures is a learning process motivated by Pavlovian components of training which are retained well, by juveniles and adults alike, over intervals typical of ontogeny of memory research.
Dev Psychobiol 1980 Sep
PMID:Retained elements of early avoidance training and relearning of forgotten operants. 740 34

Long-term potentiation (LTP) and long-term depression (LTD), often used as essential components in synaptic models for learning, memory and forgetting, can be produced in cortical tissue by repetitive activation of neural pathways under different stimulus conditions. The involvement of metabotropic glutamate receptors (mGluRs) has been postulated to be necessary for the establishment of either or both forms of synaptic plasticity in hippocampus. The recent introduction of a specific antagonist for mGluRs, (+/-)-alpha-methyl-4-carboxyphenylglycine, prompted the investigation of the respective involvement of this receptor population in the induction of LTP and LTD in visual cortex of the rat in vitro. The results suggest the critical involvement of mGluRs in producing LTD but not LTP.
Neuroreport 1994 Sep 08
PMID:Induction of LTD but not LTP through metabotropic glutamate receptors in visual cortex. 782 42

Three studies show that the retrieval process itself causes long-lasting forgetting. Ss studied 8 categories (e.g., Fruit). Half the members of half the categories were then repeatedly practiced through retrieval tests (e.g., Fruit Or_____). Category-cued recall of unpracticed members of practiced categories was impaired on a delayed test. Experiments 2 and 3 identified 2 significant features of this retrieval-induced forgetting: The impairment remains when output interference is controlled, suggesting a retrieval-based suppression that endures for 20 min or more, and the impairment appears restricted to high-frequency members. Low-frequency members show little impairment, even in the presence of strong, practiced competitors that might be expected to block access to those items. These findings suggest a critical role for suppression in models of retrieval inhibition and implicate the retrieval process itself in everyday forgetting.
J Exp Psychol Learn Mem Cogn 1994 Sep
PMID:Remembering can cause forgetting: retrieval dynamics in long-term memory. 793 Oct 95

Non-attendance at out-patient clinics, although common, has received relatively little attention. A prospective study was undertaken to assess the extent of the problem of non-attendances of newly referred dermatological patients in a single dermatological out-patient clinic over a 12-month period. The overall non-attendance rate was found to be 19%. There were no apparent significant differences between the groups of attending and non-attending patients when compared statistically. A survey of those patients who failed to attend suggested that inadequate communication between the hospital and patients (17%) and patients forgetting their appointment date (23%) may be factors that are amenable to administrative changes.
Clin Exp Dermatol 1994 Sep
PMID:An audit of the factors involved in new patient non-attendance in a dermatology out-patient department. 795 96


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