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Query: UMLS:C0233794 (memory impairment)
 7,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The reconsolidation hypothesis states that a consolidated memory could again become unstable and susceptible to facilitation or impairment for a discrete period of time after a reminder presentation. The phenomenon has been demonstrated in very diverse species and types of memory, including the human procedural memory of a motor skill task but not the human declarative one. Here we provide evidence for both consolidation and reconsolidation in a paired-associate learning (i.e., learning an association between a cue syllable and the respective response syllable). Subjects were given two training sessions with a 24-h interval on distinct verbal material, and afterward, they received at testing two successive retrievals corresponding to the first and second learning, respectively. Two main results are noted. First, the first acquired memory was impaired when a reminder was presented 5 min before the second training (reconsolidation), and also when the second training was given 5 min instead of 24 h after the first one (consolidation). Second, the first retrieval proved to influence negatively on the later one (the retrieval-induced forgetting [RIF] effect), and we used the absence of this RIF effect as a very indicator of the target memory impairment. We consider the demonstration of reconsolidation in human declarative memory as backing the universality of this phenomenon and having potential clinical relevance. On the other hand, we discuss the possibility of using the human declarative memory as a model to address several key topics of the reconsolidation hypothesis.
Learn Mem 2007 Apr
PMID:Reconsolidation of declarative memory in humans. 1752 18

Previous reports have shown that overexpression of the growth- and plasticity-associated protein GAP-43 improves memory. However, the relation between the levels of this protein to memory enhancement remains unknown. Here, we studied this issue in transgenic mice (G-Phos) overexpressing native, chick GAP-43. These G-Phos mice could be divided at the behavioral level into "spatial bright" and "spatial dull" groups based on their performance on two hidden platform water maze tasks. G-Phos dull mice showed both acquisition and retention deficits on the fixed hidden platform task, but were able to learn a visible platform task. G-Phos bright mice showed memory enhancement relative to wild type on the more difficult movable hidden platform spatial memory task. In the hippocampus, the G-Phos dull group showed a 50% greater transgenic GAP-43 protein level and a twofold elevated transgenic GAP-43 mRNA level than that measured in the G-Phos bright group. Unexpectedly, the dull group also showed an 80% reduction in hippocampal Tau1 staining. The high levels of GAP-43 seen here leading to memory impairment find its histochemical and behavioral parallel in the observation of Rekart et al. (Neuroscience 126: 579-584) who described elevated levels of GAP-43 protein in the hippocampus of Alzheimer's patients. The present data suggest that moderate overexpression of a phosphorylatable plasticity-related protein can enhance memory, while excessive overexpression may produce a "neuroplasticity burden" leading to degenerative and hypertrophic events culminating in memory dysfunction.
Learn Mem 2007 Jun
PMID:GAP-43 gene expression regulates information storage. 1755 85

Transthyretin (TTR) is a plasma and cerebrospinal fluid carrier for thyroxine and retinol, described also to sequester the amyloid beta peptide. TTR levels have been described as decreased in the cerebrospinal fluid of patients with Alzheimer's disease. In order to investigate the role of TTR in learning and memory, we studied young adult and old TTR-null 129/Sv mice for cognitive performance. In the absence of TTR, 5-month-old mice display spatial reference memory impairment when compared to age-matched wild-type mice. Interestingly, while aging in wild-type mice is associated with a worsening reference memory performance, TTR-null mice show no further impairment with increasing age. As a result, no significant differences were found in this spatial reference task in old mice. Our data show that the absence of TTR seems to accelerate the poorer cognitive performance normally associated with aging.
Neurobiol Learn Mem 2007 Oct
PMID:Transthyretin influences spatial reference memory. 1769 79

Amyloid beta peptide (Abeta) is considered one of the main agents of Alzheimer's disease pathogenesis. Recently, it has been proposed that memory deficits are caused by different stages of Abeta aggregation, particularly by oligomers. In addition, although memory impairment was found after Abeta administration in rodents and chicks, the nature of the memory deficits induced in invertebrates by acute administration of mammalian Abeta peptides is not well understood. Previously, we reported the amnesic effect of acute pre-training administration of naturally formed fibrils (NF) in crab memory. Here we evaluate the effect of NF and synthetic Abeta peptides administration at different times before and after training in this well characterized invertebrate memory model, the context-signal memory of the crab Chasmagnathus. We found a clear amnesic effect at very low doses of naturally Abeta NF only when administered immediately pre- and post-training, but not 24 h and 18 h before or 6h after training. Activation of ERK/MAPK (a protein kinase required for memory formation in this model) 60 min after administration was found. In contrast, neither JNK/SAPK nor NF-kappaB transcription factor were activated. Furthermore, synthetic Abeta1-42 and Abetapy3-42 administration induced amnesia when used after a protocol for fibrillation but not after a protocol for oligomerization. On the contrary, no amnestic effect was found when fibrillated Abeta1-40 and Abetapy11-42 peptides were used. Thus, Abeta1-42 and Abetapy3-42 peptides impaired memory and the effects were only found when highly aggregated peptides, which may include fibrils, protofibrils and oligomers, were administered. These temporally- and signaling-specific effects suggest that Abeta impairs memory by inducing transient physiological, rather than permanent neuropathological, alterations of the brain and this effect is achieved through generalized ERK activation.
Neurobiol Learn Mem 2008 May
PMID:Effect on memory of acute administration of naturally secreted fibrils and synthetic amyloid-beta peptides in an invertebrate model. 1792 Mar 4

Exposure to high altitude is known to cause impairment in cognitive functions in sojourners. The molecular events leading to this behavioral manifestation, however, still remain an enigma. The present study aims at exploring the nature of memory impairment occurring on chronic exposure to hypobaric hypoxia and the possible role of glutamate in mediating it. Increased ionotropic receptor stimulation by glutamate under hypobaric hypoxic conditions could lead to calcium mediated excitotoxic cell death resulting in impaired cognitive functions. Since glutamate is cleared from the synapse by the Glial Glutamate Transporter, upregulation of the transporter can be a good strategy in preventing excitotoxic cell death. Considering previous reports on upregulation of the expression of Glial Glutamate Transporter on ceftriaxone administration, the therapeutic potential of ceftriaxone in ameliorating hypobaric hypoxia induced memory impairment was investigated in male Sprague Dawley rats. Exposure to hypobaric hypoxia equivalent to an altitude of 7600 m for 14 days lead to oxidative stress, chromatin condensation and neuronal degeneration in the hippocampus. This was accompanied by delayed memory retrieval as evident from increased latency and pathlength in Morris Water Maze. Administration of ceftriaxone at a dose of 200 mg/kg for 7 days and 14 days during the exposure on the other hand improved the performance of rats in the water maze along with decreased oxidative stress and enhanced neuronal survival when compared to hypoxic group without drug administration. An increased expression of Glial Glutamate Transporter was also observed following drug administration indicating faster clearance of glutamate from the synapse. The present study not only brings to light the effect of longer duration of exposure to hypobaric hypoxia on the memory functions, but also indicates the pivotal role played by glutamate in mediating excitotoxic neuronal degeneration at high altitude. The therapeutic potential of ceftriaxone in providing neuroprotection in excitotoxic conditions by increasing Glial Glutamate Transporter expression and thereby enhancing glutamate uptake from the synapse has also been explored.
Neurobiol Learn Mem 2008 May
PMID:Ceftriaxone rescues hippocampal neurons from excitotoxicity and enhances memory retrieval in chronic hypobaric hypoxia. 1830 43

Purple sweet potato color (PSPC), a class of naturally occurring anthocyanins used to color food (E163), has been reported to possess a variety of biological activities, including anti-oxidant, anti-tumor, and anti-inflammatory. The effect of PSPC on the spatial learning and memory of mice treated with d-galactose (d-gal) was evaluated by the Morris water maze; d-gal-treated mice had decreased performance compared with mice in the vehicle and PSPC groups, while the PSPC+d-gal group showed significantly shortened escape latency to platform, increased swimming speed, more target quadrant search time and more platform crossings as compared with the d-gal group. Brain functions, such as memory formation and recovery of function after injury, depend on proper regulation of the expression levels of the pre- and post-synaptic proteins. We investigated the expression of four pre-synaptic proteins (growth-associated protein-43, synapsin-I, synaptophysin, and synaptotagmin) and two post-synaptic proteins (post-synaptic density protein-95 and Ca(2+)/calmodulin-dependent protein kinase II) in the hippocampus and cerebral cortex, respectively, in response to different treatments. Western blotting analysis showed that there were significant decreases in the expression of these representative synaptic proteins in the hippocampus and cerebral cortex of d-gal-treated mice. Interestingly, these decreased expression levels of synaptic proteins could be reversed by PSPC. The levels of expression of these representative synaptic proteins in mice treated with PSPC alone were not significantly different from those in untreated mice. The results of this study suggested that memory impairment and synaptic protein loss in d-gal-treated mice may be improved by treatment with PSPC.
Neurobiol Learn Mem 2008 Jul
PMID:Purple sweet potato color repairs d-galactose-induced spatial learning and memory impairment by regulating the expression of synaptic proteins. 1831 11

Hippocampal-dependent synaptic plasticity and memory are modulated by apamin-sensitive small conductance Ca2+-activated K+ (SK) channels. Transgenic mice overexpressing SK2 channels (SK2+/T mice) exhibit marked deficits in hippocampal memory and synaptic plasticity, as previously reported. Here, we examined whether SK2 overexpression affects the encoding or retention of contextual memory. Compared with wild-type littermates, SK2+/T mice exhibited significantly less context-dependent freezing 10 min and 24 h after conditioning. Interestingly, this contextual memory impairment was eliminated if SK2+/T mice were permitted longer pre-exposure to the conditioning chamber. These data support converging evidence that SK2 channels restrict the encoding of hippocampal memory.
Learn Mem 2008 Apr
PMID:Contextual memory deficits observed in mice overexpressing small conductance Ca2+-activated K+ type 2 (KCa2.2, SK2) channels are caused by an encoding deficit. 1838 75

Recent studies in patients with hippocampal lesions have indicated that the degree of memory impairment is proportional to the extent of damage within the hippocampus. Particularly, patients with damage restricted to the CA1 field demonstrate moderate to severe anterograde amnesia with only slight retrograde amnesia. Comparable results are also seen in other species such as non-human primates and rats; however, the effect of selective damage to CA1 has not yet been characterized in mice. In the present study, we investigated the effects of excitotoxic (NMDA) lesions of dorsal CA1 on several aspects of learning and memory performance in mice. Our data indicate that dorsal CA1 lesioned mice are hyperactive upon exposure to a novel environment, have spatial working memory impairments in the Y-maze spontaneous alternation task, and display deficits in an 8-arm spatial discrimination learning task. Lesioned mice are able to acquire an operant lever-press task but demonstrate extinction learning deficits in this appetitive operant paradigm. Taken together, our results indicate that lesions to dorsal CA1 in mice induce selective learning and memory performance deficits similar to those observed in other species, and extend previous findings indicating that this region of the hippocampus is critically involved in the processing of spatial information and/or the processing of inhibitory responses.
Neurobiol Learn Mem 2008 Sep
PMID:Excitotoxic lesions restricted to the dorsal CA1 field of the hippocampus impair spatial memory and extinction learning in C57BL/6 mice. 1860 45

Elucidating the functional properties of the dentate gyrus (DG), CA3, and CA1 areas is critical for understanding the role of the dorsal hippocampus in contextual fear memory processing. In order to specifically disrupt various hippocampal inputs, we used region-specific infusions of DCG-IV, the metabotropic glutamate receptor agonist, which selectively disrupts entorhinal outputs as well as mossy fiber transmission in the hippocampus. The consequences of these injections were studied using a contextual fear conditioning (CFC) paradigm. Selective contextual memory impairment was observed in DG- and CA3-, but not in CA1-treated mice. Our results emphasize the major role played by the DG and CA3 areas in the early phases of contextual memory processing, particularly during the acquisition and early consolidation phases of CFC.
Learn Mem 2009 Aug
PMID:Activation of metabotropic glutamate receptor type 2/3 supports the involvement of the hippocampal mossy fiber pathway on contextual fear memory consolidation. 1963 69

Previous research has suggested that the disruption to memory-task performance seen following acute exposure to 3,4-methylenedioxymethaphemtamine (MDMA) with rats might best be characterized as reference memory impairment rather than a working memory impairment. The current study specifically compared the effects of MDMA and scopolamine on measures of working versus reference memory in an eight-arm radial maze task. It was predicted that scopolamine would produce a greater impairment with respect to the working memory component of the task, whereas MDMA would produce a greater impairment to reference memory. On each trial rats were allowed to make a total of four arm visits in order to collect the reinforcers located at the end of different arms in the maze. Working memory errors were indicated by re-visiting an already visited arm during a trial, whereas visiting an arm that was never baited on any trial indicated a reference memory error. Using a within subjects design, rats were exposed to a range of doses of scopolamine and MDMA administered acutely. An interaction between drug type and memory error type was found. Specifically, scopolamine produced more working memory errors than reference memory errors, while MDMA produced the opposite pattern of significantly more reference memory errors compared to working memory error. This finding supported the hypothesis that MDMA disrupts reference memory processes in terms of an impairment in the strategies or rules used for solving memory tasks.
Neurobiol Learn Mem 2010 Feb
PMID:Differential effects of MDMA and scopolamine on working versus reference memory in the radial arm maze task. 1976


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