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Query: UMLS:C0002622 (amnesia)
 5,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amnesia is considered to reflect the effects of damage to a specific brain system required for elaboration, consolidation, and conscious recollection. The study of amnesia is therefore a useful approach for establishing dissociations of function and for understanding the normal organization of memory functions. Amnesic patients and two control groups were tested in two studies of priming. In the first experiment, as measured by a word completion test, all groups exhibited significant priming effects that were greater within a modality than across modalities. The amnesic patients exhibited normal priming effects both within and across modalities, despite severe impairment in recall. In the second experiment, all groups exhibited significant and equivalent priming of category exemplars when category labels were presented and subjects were asked to produce the first exemplars that came to mind. The results extend the domain in which preserved priming effects can be observed in amnesia and they suggest that features of priming observed in normal subjects describe a capacity that is independent of the brain system damaged in amnesia.
J Exp Psychol Learn Mem Cogn 1985 Apr
PMID:Priming across modalities and priming across category levels: extending the domain of preserved function in amnesia. 315 72

Certain features of abnormal memory, which have figured prominently in theoretical treatments of the amnesic syndrome, were assessed in patients with Korsakoff's syndrome, in Case N.A., and in patients receiving electroconvulsive therapy. Patients with Korsakoff's syndrome differed from the other patients by (a) failing to exhibit release from proactive interference, and (b) being disproportionately impaired in the ability to make judgments about the temporal order of recent events. These deficits appear to be related to frontal lobe damage and are superimposed on a more basic memory disorder. Theories of amnesia should be founded on the basic memory disorder and not on deficits such as these, which have no obligatory relationship to amnesia. Dissociations between aspects of memory, revealed by the study of amnesia, can also shed light on the organization of memory in the brain.
J Exp Psychol Learn Mem Cogn 1982 Nov
PMID:Comparisons between forms of amnesia: some deficits are unique to Korsakoff's syndrome. 621 21

Subjects participated in two experimental sessions designed to study laboratory-induced amnesia, one using a standard hypnosis paradigm and one using a non-hypnotic directed-forgetting paradigm. Two independent sources of variation were derived from the hypnotic amnesia data: retrieval inhibition and inhibition release. In the nonhypnotic directed-forgetting procedure, some items were cued to be forgotten shortly after presentation and some were cued to be remembered. At test, the subjects were asked to recall both the to-be-remembered and the to-be-forgotten items. Over 39% of the variance in the recall of the to-be-forgotten items could be accounted for by the inhibition and release constructs obtained with hypnosis. These relations between the two procedures were not mediated by verbal ability or cognitive style (field independence). We concluded that the mechanisms of forgetting involved in laboratory demonstrations of hypnotic and nonhypnotic amnesia are related, and the implication is that some of them are the same, namely, retrieval inhibition and inhibition release. We also argued that the possible demand characteristics that accompany the hypnosis procedure are not apparent with the nonhypnotic procedure. Therefore, the relationships observed in the present results were taken as evidence that hypnotically induced amnesia is not entirely the result of subjects' reactions to demand characteristics.
J Exp Psychol Learn Mem Cogn 1983 Oct
PMID:Mechanisms of hypnotic and nonhypnotic forgetting. 622 80

Research on alcohol amnesia has focused on memory processes that are disrupted during intoxication. The present experiment examined the possibility that certain memory processes might be resistant to the amnesic effects of alcohol. Intoxicated and sober subjects studied a list of 29 words. They were then given one of three different retention tests: free recall, identification of degraded words based on the procedure used by Warrington and Weiskrantz (1970), and yes/no recognition. As expected, free recall was significantly impaired by alcohol intoxication. In contrast, in the identification test, intoxicated subjects benefited to the same degree as sober subjects from prior exposure to the items. The two groups did not differ in immediate recognition memory. The results of the free-recall and identification tasks are similar to findings with chronic amnesic patients and suggest that perceptual fluency is not affected by alcohol, whereas elaborative processes supporting recall are particularly sensitive to disruption during intoxication. The failure to find recognition impairment at the level of intoxication used in this study distinguishes temporary alcohol amnesia from chronic amnesia.
J Exp Psychol Learn Mem Cogn 1984 Jan
PMID:Intact retention in acute alcohol amnesia. 624 32

The performance of three kinds of amnesic patients and control subjects was assessed using four methods for testing memory: free recall, recognition, cued recall, and word completion. Whereas amnesic patients were impaired on free recall, recognition, and cued recall, they were normal on word completion. Moreover, performance on the word-completion test declined at a normal rate reaching chance after about 120 min. The word-completion test resembled the cued-recall test in that the initial letters of previously presented words were given as cues. It differed from cued recall only in the instructions, which directed subjects away from the memory aspects of the test and asked them to complete each three-letter cue with the first word that came to mind. The present results offer an explanation of conflicting findings that have been obtained with amnesic patients on tests of the cued-recall type. The results are considered in terms of a process (activation or procedural learning), which is spared in amnesia and not dependent on the integrity of the damaged brain regions.
J Exp Psychol Learn Mem Cogn 1984 Jan
PMID:The information that amnesic patients do not forget. 624 34

There is substantial evidence that protein kinases, through the phosphorylation of substrate proteins, play a significant role in information processing in the brain, including processes underlying memory formation. Inhibition of the activity of the cyclic-adenosine monophosphate-dependent protein kinase A by the highly specific inhibitor, halofantrine, resulted in impairment of memory formation in day-old chicks trained on a single-trial passive avoidance task. A dose of 9.6 ng/chick halofantrine induced amnesia at the beginning of a protein synthesis-dependent long-term memory stage, the last of three stages of memory postulated to underly memory formation in the chick following passive avoidance learning. The concentration of halofantrine required for 50% inhibition of chick brain protein kinase A was found to be similar to that observed for bovine heart and rat liver. The amnestic effect of halofantrine is tentatively attributed to interference with de novo protein synthesis necessary for long-term memory consolidation. Neither anthraquinone nor the anthraquinone derivative anthraflavic acid, which have little effect on protein kinase A activity, affected memory retention. On the other hand, two other anthraquinone derivatives, chrysophanic acid and purpurin, which inhibit PKA activity, at doses of 0.25 and 0.5 ng/chick also yielded retention deficits. In these cases, however, retention losses occurred earlier than observed with halofantrine, at about 30 min post-training. The earlier effects of these inhibitors may be due to the additional inhibitory action of these compounds on protein kinase C activity, which has been demonstrated in previous studies to be implicated, possibly through phosphorylation of the GAP43 phosphoprotein, in memory processing in the stage of memory immediately preceding the protein synthesis-dependent long-term stage.
Neurobiol Learn Mem 1995 Sep
PMID:Inhibitors of cAMP-dependent protein kinase impair long-term memory formation in day-old chicks. 758 18

The effects of a nootropic drug, oxiracetam (50-100-200 mg/kg ip), and a potent antioxidant agent, ascorbic acid (62.5-125-250 mg/kg ip), administered alone or in combination, were investigated on scopolamine-induced amnesia in a mouse habituation test. The light-dark aversion test was selected and was carried out in aged mice. Habituation to the test box occurred over a 3-day period, control mice showing a significant between-day increase in the time spent in the dark box, but not in the number of transitions. On Day 4, following post-trial administration over a 3-day period of oxiracetam (50-100 and 200 mg/kg ip) or ascorbic acid (62.5-125 and 250 mg/kg ip), a significant between-day increase in the time spent in the black area, but not in the number of transitions, was found. The combination of oxiracetam (100 mg/kg ip) with ascorbic acid (125 mg/kg ip) produced a similar pattern of results. The acute administration of scopolamine (0.25 mg/kg ip) to mice treated over a 3-day period with vehicle disrupted the habituation response. In mice that had received the 3-day treatment with oxiracetam or ascorbic acid or its combination, scopolamine failed to alter significantly the learning pattern. In conclusion, these data demonstrate that ascorbic acid, alone or in combination with oxiracetam, may prevent experimentally induced amnesia in aged mice.
Neurobiol Learn Mem 1995 Sep
PMID:The effects of ascorbic acid and oxiracetam on scopolamine-induced amnesia in a habituation test in aged mice. 758 19

Amnesic patients and a control group were given a recognition test 10 min after studying words. For each recognized word, participants indicated whether they remembered it (R) or whether simply they knew that the word was presented but had no recollections about it (K). The patients were impaired for both R and K responses, performing like a control group tested after 1 week. Another control group was tested both 10 min and 1 week after study. The proportion of words initially eliciting an R response and later eliciting a K response exceeded the proportion of K responses that shifted to R responses. These data are accounted for if items initially eliciting R responses can also elicit K responses. We conclude that the R-K distinction does not reflect the operation of explicit and implicit memory but reflects instead a distinction within declarative memory. Thus, K responses depend on brain structures damaged in amnesia; R responses depend on these same structures and also on the frontal lobes for contextual information.
J Exp Psychol Learn Mem Cogn 1995 May
PMID:Remembering and knowing: two different expressions of declarative memory. 760 67

Quinacrine (QU) is an inhibitor of phospholipase A2 (PLA2). However, QU has antagonistic properties at the acetylcholine receptor as well. To investigate if PLA2 activity is of importance in memory formation, QU was tested in a passive avoidance task in the chick. Injecting QU pretraining caused amnestic effects 45 min post-training. When comparing this result with results obtained with other PLA2 inhibitors, it became apparent that QU is not acting primarily as an inhibitor of PLA2. Scopolamine, an acetylcholine receptor antagonist, was tested and produced the same onset of amnesia as QU. I conclude that QU is acting functionally as an antagonist of acetylcholine receptors rather than of PLA2.
Neurobiol Learn Mem 1995 Mar
PMID:Quinacrine acts like an acetylcholine receptor antagonist rather than like a phospholipase A2 inhibitor in a passive avoidance task in the chick. 766 95

The antibiotic anisomycin (ANI), a protein synthesis inhibitor, was used to investigate the time-related changes in protein synthesis following passive avoidance training in the day-old chick. Retention of memory for this simple learning task is known to be prevented by protein synthesis inhibitors within the first hour post-training. Here we report a second, later time window during which inhibition of protein synthesis results in amnesia following one-trial passive avoidance training. Birds were given bilateral intracranial injections of ANI (10 microliters/hemisphere of a 30 mM solution) at various times relative to training and tested 24 h later. Injections given between 0.5 h prior to 1.5 h post-training or 4-5 h post-training, but not at later or at intervening times, resulted in amnesia. These results are discussed in the context of earlier findings, using the inhibitor of glycoprotein synthesis 2-deoxygalactose, that memory formation shows two glycoprotein-synthesis-dependent periods of sensitivity (Scholey, Rose, Zamani, Bock, & Schachner, 1993). The time windows of susceptibility of ANI and 2-Dgal are consistent with a model in which there are two waves of neural activity following training; during the second, commencing 4 h after training, proteins are synthesized and then glycosylated as part of the establishment of an enduring memory trace.
Neurobiol Learn Mem 1995 May
PMID:Two time windows of anisomycin-induced amnesia for passive avoidance training in the day-old chick. 767 Aug 43


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