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Query: UMLS:C0751295 (memory loss)
 3,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most current models of memory predict that the presence of increasingly well-learned, or strong, items in memory will cause increasing interference. This phenomenon, the list-strength effect, occurs as predicted when memory is tested by free recall but not when a recognition test is used. Four experiments use end-of-session testing to demonstrate that redistribution of storage time or effort from strong to weak items on mixed lists does not occur and therefore cannot be masking interference by strong items. Delay between study and test is found to cause memory loss independent of the basic list-strength findings. It is concluded that the presence of strong items in memory does not interfere with recognition performance and that interference is due to failures of retrieval rather than to composition or other forms of destructive interaction during storage.
J Exp Psychol Learn Mem Cogn 1991 Sep
PMID:Interference and the representation of events in memory. 183 68

Two experiments on same-different vowel discrimination are reported. In each, the main variable was the duration of a silent delay between the two items being judged. As would be expected from the assumption that such judgements depend at least partly on auditory sensory memory, longer delays led to poorer discrimination than shorter delays. The auditory memory loss seems to be asymptotic at about 3 sec, whether it is measured by correct discrimination of (as in one part of Experiment 2) by the contextual influence of the first vowel on identification of the second.
J Exp Psychol Learn Mem Cogn 1982 Mar
PMID:Decay of auditory memory in vowel discrimination. 621 Jul 49

Day-old chicks trained on a single trial passive avoidance learning task showed a significant increase, relative to untrained controls, in activity of the Ca2+/calmodulin-dependent protein kinase (CaMK) in the particulate fraction from tissues from the intermediate medial hyperstriatum ventrale region of the forebrain. The increased kinase activity was observed within 10 min following training and persisted for at least 70 min posttraining. Amnesia for the task was induced by micromolar concentrations of the specific CAMK II antagonist, KN-62, administered into the neostriatal/hyperstriatal region of the forebrain. The effect of KN-62 was lateralized. In the right hemisphere, KN-62 induced amnesia only when injected within 2. 5 min following training, with memory loss evident by 5 min posttraining. In contrast, in the left hemisphere amnesia was induced by KN-62 administered as late as 5 min posttraining, with onset of amnesia occurring after 10 min posttraining. The findings were interpreted within the context of a three-stage model of memory formation.
Neurobiol Learn Mem 1996 Jul
PMID:The involvement of Ca2+/calmodulin-dependent protein kinase in memory formation in day-old chicks. 866 Dec 48

In 1929, H.C. Blodgett reported the results of a seminal maze learning experiment using rats. In that experiment, hungry rats ran in a complex maze but were not rewarded on reaching the goal box. Not surprisingly, the performance of the hungry rats did not improve over trials. However, with the introduction of reward, the error scores of the rats suddenly dropped to the level of the control rats that were rewarded from the outset. This finding indicates that the experimental group had learned the maze despite the absence of reward but that the learning was latent rather than manifest. With Blodgett's findings, the distinction between learning and performance became firmly established, if not as widely appreciated as it might be. Blodgett's (1929) early experimental finding of latent learning could well serve as a paradigm for the approach taken here. That is, we have emphasized the principle that a lack of performance does not necessarily indicate a lack of either learning or memory. This principle is much more than an empty admonition: We have shown it can have a firm theoretical basis, one that has been confirmed repeatedly by experiments cited throughout this paper. That is, it has been shown numerous times that a failure to perform either in a Pavlovian or instrumental learning task or to remember in an animal or human memory task under one set of conditions could be alleviated under another set of conditions. Forgetting was viewed here as a failure of performance resulting from the cues at test retrieving a memory other than the target memory or retrieving no memory at all. According to this view, memory involves discrimination learning. Essentially, memories are stored in the presence of an elaborate set of interoceptive and exteroceptive stimuli, a context. Whether at test the target memory is retrieved depends on how well the cues at test discriminate between the target memory and other memories. This approach suggests that forgetting does not occur: There is only a failure to perform because of a difference between the stimulus conditions prevailing at encoding and at test. It was demonstrated that this approach is at least as reasonable as that which suggests that true forgetting occurs, but certainly more useful. At least three advantages adhere to our view that memory is a discrimination problem. First, in almost numberless cases, it has been shown that failure of performance under one set of stimulus conditions can be alleviated under some other set of stimulus conditions. Second, the proposition that altered stimulus conditions are responsible for forgetting is one of wide generality. Thus, the altered stimulus conditions approach can serve as an explanation not only for various human memory findings but also for various animal memory and learning findings. Finally, and perhaps most importantly, the present approach provides investigators with a powerful and proven working hypothesis. It tells us not to accept failures of performance as indicating an absence of learning or a loss of memory but rather to seek conditions favorable to improving performance, a strategy that should lead to a better fundamental understanding of memory and learning. This position is obviously a type of optimality theory, of which evolutionary theory is one of the more outstanding examples. In optimality theory, any deviation from some ideal state or condition prompts the investigator to seek the reasons for deviation. This approach may prove as successful when applied to learning and memory as it has to other areas of science.
Learn Mem
PMID:Remembering and forgetting as context discrimination. 1046 70

Although mild progressive memory impairment is commonly associated with normal human aging, it is unclear whether this phenomenon can be explained by specific structural brain changes. In a research sample of 54 medically healthy and cognitively normal elderly persons (ages 55-87, x = 69.0 +/- 7.9), magnetic resonance imaging (MRI) was used to derive head-size-adjusted measurements of the hippocampal formation (HF) (dentate gyrus, hippocampus proper, alveus, fimbria, subiculum), the superior temporal gyrus (STG), and the subarachnoid cerebrospinal fluid (CSF) (to estimate generalized cerebral atrophy). Subjects were administered tests of primary memory (digit span) and tests of secondary memory with immediate and delayed recall components (paragraph, paired associate, list recall; facial recognition). Separate composite scores for the immediate and delayed components were created by combining, with equal weighting, the subtests of each category. The WAIS vocabulary subtest was used as a control measure for language and intelligence. A highly significant correlation (P < 0.001), independent of age, gender, and generalized cerebral atrophy was found between HF size and delayed memory performance. No significant correlations were found between HF size and primary or immediate memory performance. STG size was not significantly correlated with any of the composite memory variables. These results suggest that HF atrophy may play an important independent role in contributing to the memory loss experienced by many aging adults.
Learn Mem
PMID:Hippocampal formation size in normal human aging: a correlate of delayed secondary memory performance. 1046 85

Previous studies with general inhibitors of nitric oxide synthase have yielded variable and contradictory results with respect to their effects on memory. This may have been due to differential effects of blocking the various isoforms of this enzyme. We show that day-old chicks trained on a single-trial passive-avoidance task suffered significant memory loss from approximately 40 min post-training following post-training intracranial administration of a potent inhibitor of eNOS. Administration of a specific nNOS or iNOS inhibitor at the same time had no effect on retention, although a role for either of these isoforms when administered at a different time after learning has yet to be fully investigated. The onset of memory loss following eNOS inhibition is the same as observed following general NOS inhibition, which suggests that amnestic effects observed in previous studies using nonspecific inhibitors may be attributable to blocking the function of eNOS. The findings indicate that eNOS may play a role in memory formation for this task, which is at least distinct from any role that may be played by nNOS.
Learn Mem
PMID:Inhibition of the endothelial isoform of nitric oxide synthase impairs long-term memory formation in the chick. 1054 66

Recent advances in behavioral analyses of transgenic mouse models of Alzheimer's disease (AD) are discussed, and their impact on our understanding of the molecular basis of cognitive impairment in AD is considered. Studies of the relationship between memory and A Beta in transgenic mice expressing the amyloid precursor protein (APP) and its variants suggest that aging promotes the formation of soluble A Beta assemblies mediating negative effects on memory. A significant component of memory loss in APP transgenic mice is apparently caused by soluble A Beta assemblies, but whether and how much of the dementia within individuals afflicted with AD is caused by these A Beta species is unclear. Future studies in composite transgenic mice developing amyloid plaques, neurofibrillary tangles, and other AD pathology may allow for the determination of the relative contribution of A Beta and non-A Beta components to dementia.
Learn Mem
PMID:Learning and memory in transgenic mice modeling Alzheimer's disease. 1177 29

The cytosolic posttranslational protein-modifying mechanism of monoADP-ribosylation has been implicated in long-term potentiation, a synaptic model of memory formation. The current study investigated the effect of inhibiting mono(ADP-ribosyl) transferase on memory for the passive avoidance task in day-old chicks (white Leghorn-black Australorp). Various doses of novobiocin or menadione sodium bisulfite were administered intracranially at different times before or after training. Control chicks were administered saline at matched times. Novobiocin (650 microM) or menadione sodium bisulfite (250 microM) administered between 5.0 min pretraining and 2.5 min posttraining was found to cause a persistent loss of retention from 120 min posttraining. These data provide the first demonstration that monoADP-ribosylation is required for the maintenance of long-term memory. Furthermore, the temporal characteristics of the memory loss caused by monoADP-ribosylation inhibition appears to exclude this mechanism as a downstream effect of the well-established nitric oxide activity previously shown to occur within 40 min of passive avoidance training.
Neurobiol Learn Mem 2002 Jul
PMID:Inhibition of monoADP-ribosylation prevents long-term memory consolidation of a single-trial passive avoidance task in the day-old chick. 1207 76

Bilateral administration of nitric oxide synthase inhibitors into the intermediate medial hyperstriatal (IMHV) region of the chick brain impairs memory formation for an avoidance task. The aim of the current study was to determine whether this effect was restricted to a particular location in the brain, and whether inhibition was equally effective in both hemispheres. White Leghorn x black Australorp chicks were administered 0.5 mM N(omega)-Nitro-L-arginine methyl ester bilaterally into the lobus parolfactorius (LPO), or unilaterally into the IMHV. Injections into the LPO between 5 min pre-training and 40 min post-training had no effect on retention. In contrast, unilateral injections into the IMHV impaired retention and memory loss occurred from 40 min post-training. The effective administration time was hemisphere-dependent, requiring left hemisphere administration around the time of training and right hemisphere administration between 15 and 25 min post-training. These data suggest that localized nitric oxide activity in each hemisphere of the chick brain is necessary for the consolidation of memory for this task.
Neurobiol Learn Mem 2003 May
PMID:Effects of nitric oxide inhibition on avoidance learning in the chick are lateralized and localized. 1267 24

Previous research has indicated a role for both the neuronal (nNOS) and endothelial (eNOS) nitric oxide isoforms in memory formation. In addition, two distinct periods of activity of nitric oxide activity, dissociated by hemispheric localization, are implicated following passive avoidance training in the chick. In the present study, we trained black Australorp-white Leghorn chicks on a color discrimination avoidance task. Diphenyleneiodonium chloride (1 microM) or N-propyl-l-arginine (50 microM) was administered into either the left or right hemisphere of the chick brain in an attempt to differentiate the effects of inhibiting eNOS or nNOS, respectively. The memory loss previously observed following administration of diphenyleneiodonium chloride between 10 and 20 min posttraining was found to be lateralized to the right hemisphere, although administration of this agent into the left hemisphere around the time of training was also amnestic. In contrast, N-propyl-l-arginine caused memory loss only when administered to the left hemisphere around the time of training. These findings suggest that activation of both eNOS and nNOS isoforms may be essential for long-term memory consolidation of this task. Further, these two periods of activity are defined temporally and by hemisphere localization, although confirmation with more selective inhibitors when they become available is advised.
Learn Mem
PMID:Hemispheric dissociation of the involvement of NOS isoforms in memory for discriminated avoidance in the chick. 1455 3


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