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At least 757 records · Page 42Linked to original sources
PubMed2004

Effects of aversive stimuli on learning and memory in Arctic ground squirrels.

The present study was designed to assess effects of aversive stimuli on learning and memory in wild-caught Arctic ground squirrels (AGS, Spermophilus parryii) using an active avoidance learning paradigm. Results indicate that animals trained with low-value aversive stimuli (air puffs and lights) retained the task better than animals trained with high-value aversive stimuli (air puffs, lights, and foot shock). Poor retention could not be explained by learning impairment, fear-induced freezing behavior or the effects of massed versus spaced training trials. Wild-caught AGS readily hibernate under laboratory conditions and provide a model of pronounced adult synaptic plasticity associated with emergence from hibernation. Characterization of learning and retention using active avoidance as well as other learning paradigms is a first step towards developing behavioral paradigms to assess cognitive function in this wild-trapped species. The present study shows that captive AGS are sensitive to aversive stimuli, argues for a direct effect on retention and suggests that high baseline levels of stress in a captive population may influence behavioral measures. The results further suggest that future studies of the effects of hibernation on learning and retention of active avoidance tasks employ low-level aversive stimuli.

Animals↗
PubMed1988

The neurobiology of learning and memory: elucidation of the mechanisms of cognitive dysfunction.

This paper reviews evidence which suggests that there is a series of events at the synaptic level, beginning with synaptic activation, responsible for the formation of memories. Synaptic use above routine levels activates NMDA receptors which allows calcium influx into the neuron. Calcium appears to trigger changes in synapse and synaptic terminal shape (via cytoskeletal activation), and an increase in synaptic size (via new protein synthesis). New synapses ultimately form either de novo or by splitting, and new dendritic spines and dendritic length is added. Several forms of cognitive dysfunction, such as Downs syndrome, aging and Alzheimer's disease, and exposure to the neurotoxins lead or aluminum appear to involve, at least in part, disruptions in this process. Evidence is reviewed to support the theory that memories may involve alterations in specific sets of synapses located at specific dendritic locations; this theory may explain some of the learning and memory deficits seen in conditions resulting in cognitive dysfunction.

Cognition Disorders↗
PubMed2005

Targeting amyloid-beta peptide (Abeta) oligomers by passive immunization with a conformation-selective monoclonal antibody improves learning and memory in Abeta precursor protein (APP) transgenic mice.

Passive immunization of murine models of Alzheimer disease amyloidosis reduces amyloid-beta peptide (Abeta) levels and improves cognitive function. To specifically address the role of Abeta oligomers in learning and memory, we generated a novel monoclonal antibody, NAB61, that preferentially recognizes a conformational epitope present in dimeric, small oligomeric, and higher order Abeta structures but not full-length amyloid-beta precursor protein or C-terminal amyloid-beta precursor protein fragments. NAB61 also recognized a subset of brain Abeta deposits, preferentially mature senile plaques, and amyloid angiopathy. Using NAB61 as immunotherapy, we showed that aged Tg2576 transgenic mice treated with NAB61 displayed significant improvements in spatial learning and memory relative to control mice. These data implicated Abeta oligomers as a pathologic substrate for cognitive decline in Alzheimer disease.

Alzheimer Disease↗
PubMed2005

Early protein malnutrition changes learning and memory in spaced but not in condensed trials in the Morris water-maze.

Early protein malnutrition induces structural, neurochemical and functional changes in the central nervous system leading to alterations in cognitive and behavioral development of rats. The aim of the present study was to investigate the effects of protein malnutrition during lactation on acquisition and retention of spatial information using different training procedures (spaced x condensed trials). Rats treated with 16% (well-nourished) or 6% (malnourished) protein diets during the lactation phase and nutritionally recovered until 70 days of age were tested in the Morris water-maze in procedures of 1 trial/day (spaced trials), 4, 8, 12 trials/day (intermediate density) and 24 trials/day (condensed trials), completing 24 trials at the end of training. Seven and 28 days after the training the animals were tested again in just one trial to assess long-term memory. The results showed that protein malnutrition caused deficits on the spatial learning and memory in spaced but not in intermediate and condensed trials procedure. Seven and 28 days after the training there was an increase in the latency to find the platform but only malnourished animals submitted to 1 trial/day had significantly higher latency as compared with well-nourished controls. One of the possible hypotheses is that the effect protein malnutrition only in the procedure of spaced trials could be due to deficits in memory consolidation. It is suggested that these deficits can be the result of alterations produced by protein malnutrition in the hippocampal formation or in long-lasting emotional and/or motivational aspects of the rat's behavior.

Aging↗
PubMed2003

Verbal learning and memory in schizophrenic and Parkinson's disease patients.

The purpose of this study was to investigate the neurofunctional substrate of verbal learning and memory impairments in schizophrenic patients. In this pilot study, our aim was to compare the memory disturbance of schizophrenic patients to the subcortico-frontal memory profile of Parkinson's disease (PD) patients. The California Verbal Learning Test, a verbal episodic memory test, was administered to 60 subjects, 20 patients with schizophrenia, 20 patients with PD and 20 healthy control subjects. All subjects were aged between 50 and 70 years and all patients were in a stable phase. Like the Parkinson patients, the schizophrenic patients showed a major deficit of retrieval characterized by deficit of recalls but contrarily to PD patients, schizophrenic patients' encoding scores were altered. These impairments in episodic memory could suggest a dysfunction of the subcortico-frontal circuits in schizophrenic patients. However, they demonstrated an additional encoding deficit associated with probable frontal in situ alteration.

Aged↗
PubMed1999

Borna disease virus-induced hippocampal dentate gyrus damage is associated with spatial learning and memory deficits.

In neonatally inoculated rats, Borna disease virus (BDV) leads to a persistent infection of the brain in the absence of an inflammatory response and is associated with neuroanatomic, developmental, physiologic, and behavioral abnormalities. One of the most dramatic sites of BDV-associated damage in the neonatal rat brain is the dentate gyrus, a neuroanatomic region believed to play a major role in spatial learning and memory. The absence of a generalized inflammatory response to neonatal BDV infection permits direct effects of viral damage to the dentate gyrus to be examined. In this report, neonatally BDV-infected rats at various stages of dentate gyrus degeneration were evaluated in the Morris water maze, a swimming test that assesses the rats' capacity to navigate by visual cues. Our data demonstrate progressive spatial learning and memory deficits in BDV-infected rats that coincided with a gradual decline in the estimated hippocampal dentate gyrus neuron density.

Animals↗
PubMed1992

Evaluation of learning and memory mechanisms employing elevated plus-maze in rats and mice.

1. The effect of drugs affecting learning and memory was investigated using transfer latency (TL) as parameter for acquisition and retention of memory process on elevated plus-maze both in rats and mice. Further the validity of the procedure was envisaged. 2. The results provide an evidence for utility of shortened TL on 2nd day trial in old rats and mice as a parameter for retention or consolidation of memory, while treatment of drugs 30 min prior to 1st day may also be utilised for acquisition related action of drugs. 3. The drugs producing acquisition deficits namely scopolamine (0.1-0.5 mg/kg) and MK 801 (0.05-0.1 mg/kg) did not affect the shortened TL on elevated plus-maze in rats while nootropics, like piracetam (150 mg/kg) and captopril (30 mg/kg) reduced the shortened TL. The memory enhancing effect of these agent was reversed by scopolamine (0.3 mg/kg) and MK 801 (0.1 mg/kg) both in rats and mice. The results suggested the acquisition affecting drugs, however, did not show any effect on retention parameter (shortened TL) but can reverse the retention facilitatory action of nootropics. The results also provide indirect evidence for participation of cholinergic and NMDA-receptor blockade in the mechanism of these drugs. 4. Scopolamine and MK 801 produced acquisition deficits in mice, as they increased the TL on 1st and 2nd day trial while physostigmine (0.05 mg/kg) decreased the 2nd day TL. Physostigmine (0.1 mg/kg) reversed scopolamine and MK 801 induced acquisition deficits suggested participation of cholinergic and NMDA- receptor in learning process. 5. The results validate the utility of the elevated plus-maze for evaluation of possible nootropic action of drugs.

Aging↗
PubMed1997

Protein kinase C, learning and memory: a circular determinism between physiology and behaviour.

1. In vertebrates as in invertebrates, protein kinase C appears to have a key role in learning and memory, probably given its involvement in synaptic plasticity. 2. Hippocampal PKC in mammalians is activated by learning in a large variety of memory tasks. However, the kind of information processed, the type of task, and the dynamics of learning processes all induce differential changes in the mode of PKC activation and in its anatomy. 3. The behaviourally induced changes in PKC activity are often varying in their magnitude. Inter-individual differences in PKC basal activity are generally correlated to the ability to learn. 4. Pharmacologic activation and inhibition of brain PKC shows that PKC activation plays an important role in cognitive function. 5. Basal PKC stores characterising each individual could be determined by genetic factors and modulated through life by individual experience. 6. The issue of PKC and memory relationships is reformulated through a comprehensive interactionist model which leads to formulating some new testable predictions.

Animals↗
PubMed2005

Transient prenatal vitamin D deficiency is associated with subtle alterations in learning and memory functions in adult rats.

Based on clues from epidemiology, low prenatal vitamin D has been proposed as a candidate risk factor for schizophrenia. Recent animal experiments have demonstrated that transient prenatal vitamin D deficiency is associated with persistent alterations in brain morphology and neurotrophin expression. In order to explore the utility of the vitamin D animal model of schizophrenia, we examined different types of learning and memory in adult rats exposed to transient prenatal vitamin D deficiency. Compared to control animals, the prenatally deplete animals had a significant impairment of latent inhibition, a feature often associated with schizophrenia. In addition, the deplete group was (a) significantly impaired on hole board habituation and (b) significantly better at maintaining previously learnt rules of brightness discrimination in a Y-chamber. In contrast, the prenatally deplete animals showed no impairment on the spatial learning task in the radial maze, nor on two-way active avoidance learning in the shuttle-box. The results indicate that transient prenatal vitamin D depletion in the rat is associated with subtle and discrete alterations in learning and memory. The behavioural phenotype associated with this animal model may provide insights into the neurobiological correlates of the cognitive impairments of schizophrenia.

Analysis of Variance↗
PubMed1998

The distribution of nitric oxide synthase-I and NADPH-diaphorase containing neurons in the cerebral cortex of different strains of mice and its association with learning and memory.

We investigated the distribution of nitric oxide synthase-I (NOS-I) containing neurons within the neocortex of inbred mice belonging to the Balb/c, NMRI and DBA/2 strains which differ in learning and memory performance. The NOS-I positive neurons were detected immunohistochemically with antibodies against NOS-I and enzyme histochemically using their NADPH-diaphorase (NADPH-d) activity. The qualitative and quantitative evaluation of cortical NADPH-d and NOS-I containing neurons revealed that more than 95% of these cells contained both enzymes. Therefore, we combined the NADPH-d with the WFA-staining to evaluate and parcellate at one section. The specific differences in learning and memory tasks of the three mouse strains have been tested in previous studies. Our investigation test the hypothesis that differences in various aspects of eight-arm radial maze learning are associated with differences in the density of NOS-I positive neurons in cytoarchitectonically and functionally identified cortical areas. We found an increased density of NADPH-d neurons within the whole neocortex in the DBA/2 strain, which reached a lower learning score than the Balb/c and NMRI strains. Significantly higher densities of NADPH-d neurons appeared in the areas of the gustatory cortex, the piriform cortex, the entorhinal cortex and in area 1 of the temporal cortex in DBA/2 mice. A negative correlation exists between the learning scores and the number of NADPH-d positive neurons. If NOS-I activity influences spatial learning as determined in the eight-arm radial maze, the areas with strongly elevated NADPH-d positive neurons may demarcate task-related cortical areas affected in mice with a reduced learning capacity.

Animals↗
PubMed2006

Forebrain-specific knockout of B-raf kinase leads to deficits in hippocampal long-term potentiation, learning, and memory.

Raf kinases are downstream effectors of Ras and upstream activators of the MEK-ERK cascade. Ras and MEK-ERK signaling play roles in learning and memory (L&M) and neural plasticity, but the roles of Raf kinases in L&M and plasticity are unclear. Among Raf isoforms, B-raf is preferentially expressed in the brain. To determine whether B-raf has a role in synaptic plasticity and L&M, we used the Cre-LoxP gene targeting system to derive forebrain excitatory neuron B-raf knockout mice. This conditional knockout resulted in deficits in ERK activation and hippocampal long-term potentiation (LTP) and impairments in hippocampus-dependent L&M, including spatial learning and contextual discrimination. Despite the widespread expression of B-raf, this mutation did not disrupt other forms of L&M, such as cued fear conditioning and conditioned taste aversion. Our findings demonstrate that B-raf plays a role in hippocampal ERK activation, synaptic plasticity, and L&M.

Animals↗
PubMed2000

DNA fragmentation factor 45 deficient mice exhibit enhanced spatial learning and memory compared to wild-type control mice.

Programmed cell death or apoptosis is a highly regulated physiological process that is critical in development, particularly in the central nervous system. The DNA fragmentation factor 45 (DFF45 or ICAD) is a subunit of a heterodimeric DNase complex that is crucial for DNA fragmentation and normal apoptosis. To examine the neurobiological consequences of lacking DNA fragmentation and timely apoptosis during mouse development in vivo, we compared spatial learning behaviors in DFF45 mutant and wild-type control mice. We found that DFF45 mutant mice exhibit enhanced spatial learning and memory compared to wild-type mice. Moreover, both the granule cell density and total granule cell number in the hippocampal dentate gyrus region are higher in the DFF45 mutant brains than in the wild-type brains. We propose that the increase in granule cell number in the dentate region due to the DFF45 mutation changes the neuronal network underlying spatial learning and memory in DFF45 mutant mice.

Animals↗
PubMed2001

Gene targeting reveals a role for the glutamate receptors mGluR5 and GluR2 in learning and memory.

This work suggests that class I mGluRs are involved in long-term potentiation (LTP) at CA1 synapses within the hippocampus. Our data support a pathway linking class I-mGluRs with PKC and src to enhance the open probability of the NMDAR channel. This leads to LTP of the NMDAR, but not the AMPAR. We are currently analyzing double mGluR1 X mGluR5 knockouts with Collingridge for a loss of the LTP induction switch [Nature 368 (1994) 740.]. This induction of LTP of the NMDAR is necessary for "spatial" learning and memory to occur, since mice lacking the mGluR5 are deficient in the Morris water maze and context-dependent fear conditioning. We postulate that AMPARs may provide negative feedback inhibition to the NMDAR. Hence, in null mutants lacking the AMPAR subtype, GluR2, LTP in the CA1 region of hippocampal slices was markedly enhanced (twofold) and non-saturating, whereas neuronal excitability and paired-pulse facilitation were normal. The ninefold increase in Ca(2+) permeability, in response to kainate application, suggests one possible mechanism for enhanced LTP. Enhanced LTP could result from enhanced AMPAR channel conductance or increased recruiting of previously silent synapses. Since the GluR2 null mutants showed reduced exploration and impaired motor coordination, we could make no conclusion about its role in learning and memory. Future work will be directed to inducible deletion of GluR2 only in CA1 after development is complete. These results support the correlation between LTP and learning and memory.

Animals↗
PubMed2004

[Protection of zinc and selenium content of brain and blood on learning and memory exposed to lead in growing rats].

OBJECTIVE: The purpose of this paper was to explore the relations between lead levels of brain and blood on learning and memory, and to determine the antagonization of selenium and zinc on lead toxicity in brain and blood. METHODS: The growing rats were fed with diet added with different levels of selenium, zinc and lead for 12 weeks. RESULTS: (1) The lead levels of brain and blood of rats exposed to lead was higher than that of the control group; the lead levels of brain and blood administrated lead decreased following the increased in selenium and zinc levels in the diet. (2) Error frequencies and total time in water-maze significantly reduced in the groups exposed to lead. (3) Error frequencies and total time in water-maze and lead levels of brain and blood presented positive relation. CONCLUSION: The present study indicated that supplementary suitable zinc or/and selenium could alleviate the lead toxicity on the brain and blood of rats.

Animals↗
PubMed2001

3,4-methylenedioxymethamphetamine (ecstasy)-induced learning and memory impairments depend on the age of exposure during early development.

Use of 3,4-methylenedioxymethamphetamine (MDMA; ecstasy) has increased dramatically in recent years, yet little is known about its effects on the developing brain. Neonatal rats were administered MDMA on days 1-10 or 11-20 (analogous to early and late human third trimester brain development). MDMA exposure had no effect on survival but did affect body weight gain during treatment. After treatment, body weight largely recovered to 90-95% of controls. MDMA exposure on days 11-20 resulted in dose-related impairments of sequential learning and spatial learning and memory, whereas neonatal rats exposed on days 1-10 showed almost no effects. At neither stage of exposure did MDMA-treated offspring show effects on swimming ability or cued learning. Brain region-specific dopamine, serotonin, and norepinephrine changes were small and were not correlated to learning changes. These findings suggest that MDMA may pose a previously unrecognized risk to the developing brain by inducing long-term deleterious effects on learning and memory.

3,4-Methylenedioxyamphetamine↗
PubMed2003

Cholecystokinin and learning and memory processes.

Cholecystokinin (CCK) is a classical brain-gut peptide that exerts a variety of physiological actions in the gastrointestinal tract and central nervous system. CCK occurs in several molecular forms of varying aminoacid length, the sulphated octapeptide (CCK-8) being the predominant form in the brain. CCK mediates its effects through interaction with specific receptors subdivided in two subtypes--CCK-A (present in the periphery and in few selected brain nuclei) and CCK-B (the predominant receptor subtype in the brain). CCK is implicated in variety of behavioral functions as satiety, anxiety, exploratory and locomotor activity and learning and memory. After a brief description of the distribution, molecular forms, release, inactivation, etc. of CCK in the brain, the present review summarizes the recent data on the role of CCK in learning and memory. The memory-enhancing effects of CCK have been demonstrated in various types of memory. Data showing that CCK-A receptors mediate mnemonic while CCK-B receptors mediate amnestic effects are also presented.

Animals↗
PubMed1998

[Memory and learning abilities in everyday life of the elderly].

Self-evaluations by adults (varying in age from 45-92 years) of their memory and learning abilities were investigated and related to performance on laboratory and ecological memory tasks. Hardly any association was found between subjective and objective measures. Self-evaluations were strongly influenced by (systematically varied) frames of reference: optimistic in comparisons with other people, pessimistic in comparisons with their own previous level of functioning. The most frequent problems were 'learning something new' and 'remembering names'. In contrast to external memory aids, cognitive strategies were rarely used spontaneously. Strategy training led to significant improvement of performance, that remained stable at follow-up. A further opportunity for improving performance was realized by ergonomic adaptations of computerized systems (teleshopping). Problems in learning to use such systems were strongly reduced by decreasing the load on working memory and by adapting the system to existing knowledge and skills of the users. A general observation in the different projects was that age-differences could explain only a small percentage of the variance in subjective and objective memory measures.

Adaptation, Psychological↗
PubMed1986

Effects of oxiracetam on learning and memory in animals: comparison with piracetam.

The effects of oxiracetam and piracetam were compared in learning and memory tests in rats and mice. In the dose range examined, the two nootropics were equally active in reducing the amnesia induced by cerebral electroshock in the mouse. Step-down retention performance, however, was distinctly improved by oxiracetam but unaffected by piracetam, no matter whether it was given before or immediately after the learning trial. Oxiracetam also improved acquisition performance in aged (24- to 27-month-old) rats in an active-avoidance situation at doses of 30 and 100 mg/kg i.p. whereas piracetam showed no effect at 100 mg/kg i.p.

Aging↗