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PubMed1998

Reward-produced memories regulate memory-discrimination learning, extinction, and other forms of discrimination learning.

In memory-discrimination learning, reward-produced memories are differentially rewarded such that they are the only stimuli available to support discriminative responding. Memory-discrimination learning was used in this study as follows: Reward-produced memories that were assumed to regulate instrumental performance in previously reported extinction and discrimination learning investigations were isolated and explicitly differentially reinforced (prior to a shift to extinction) in each of 4 runway investigations with rats. Results obtained here in the explicit discrimination learning stage and in the subsequent extinction stage were consistent with the prediction of the memory view and with prior discrimination learning and extinction findings. The memory interpretation was applied to memory-discrimination learning, to extinction, and to 2 other types of discrimination learning. It appears that a theory must use reward-produced memories to explain all 4 types of discrimination learning.

Animals↗
PubMed2000

Spatial memory and learning deficits after experimental pneumococcal meningitis in mice.

Survivors of bacterial meningitis frequently suffer from long-term sequelae, particularly from learning and memory deficits. For this reason, spatial memory and learning was studied in a mouse model of ceftriaxone-treated Streptococcus pneumoniae meningitis. Persistent deficits of spatial learning despite normal motor function were observed in mice infected with 10(4) colony-forming units (CFU) in 25 microl of saline into the right forebrain in comparison to mice treated with an equal amount of saline. Survivors of meningitis performed significantly worse in memorizing a hidden platform in a Morris water maze. After 2 weeks, the difference between post-meningitis and control mice diminished. Yet, when the platform was moved after 180 days, learning of the new location was still strongly impaired in mice surviving meningitis.

Animals↗
PubMed1998

A four year prospective study of age-related cognitive change in adults with Down's syndrome.

BACKGROUND: While neuropathological studies indicate a high risk for Alzheimer's disease in adults with Down's syndrome, neuropsychological studies suggest a lower prevalence of dementia. In this study, cognitive deterioration in adults with Down's syndrome was examined prospectively over 4 years to establish rates and profiles of cognitive deterioration. METHODS: Fifty-seven people with Down's syndrome aged 30 years or older were assessed using a battery of neuropsychological tests on five occasions across 50 months. Assessments of domains of cognitive function known to change with the onset of Alzheimer related dementia were employed. These included tests of learning, memory, orientation, agnosia, apraxia and aphasia. The individual growth trajectory methodology was used to analyse change over time. RESULTS: Severe cognitive deterioration, such as acquired, apraxia and agnosia, was evident in 28.3% of those aged over 30 and a higher prevalence of these impairments was associated with older age. The rate of cognitive deterioration also increased with age and degree of pre-existing cognitive impairment. Additionally, deterioration in memory, learning and orientation preceded the acquisition of aphasia, agnosia and apraxia. CONCLUSIONS: The prevalence of cognitive impairments consistent with the presence of Alzheimer's disease is lower than that suggested by neuropathological studies. The pattern of the acquisition of cognitive impairments in adults with Down's syndrome is similar to that seen in individuals with Alzheimer's disease who do not have Down's syndrome.

Adult↗
PubMed2005

Steady-state pharmacokinetics and pharmacodynamics of CHF3381, a novel antineuropathic pain agent, in healthy subjects.

AIMS: To evaluate the safety, tolerability, pharmacokinetic and pharmacodynamic profiles of CHF3381, a dual NMDA and MAO-A inhibitor, after multiple oral doses in healthy subjects. METHODS: Forty-eight young males received CHF3381 at doses of 100 mg twice daily, 200 mg twice daily, 400 mg twice daily or placebo for 2 weeks according to a double-blind, randomized, parallel group design. Plasma and urine concentrations of the parent drug and of two major metabolites (CHF3567 and 2-aminoindane) were measured over time. MAO-A activity in plasma was estimated by measuring plasma concentrations of 3,4-dihydroxyphenylglycol. Sustained attention, memory and sedation were assessed throughout the study with standard psychometric tests. RESULTS: Most of the adverse events were mild in intensity, with dose regimens of 100 mg twice daily and 200 mg twice daily being indistinguishable from placebo. After 400 mg twice daily, the most frequent adverse events were mild dizziness, asthenia and insomnia. At steady-state, 400 mg twice daily slightly increased supine heart rate (+ 9 +/- 2 beats min(-1)) and diastolic blood pressure (+6 +/- 2 mmHg) compared with placebo. There were no dose-dependent or consistent effects of CHF3381 on attention, motor co-ordination or memory, but 400 mg twice daily significantly decreased alertness compared with placebo. Plasma concentrations of CHF3381 peaked at around 3 h and were dose-proportional. The elimination half-life of CHF3381 was estimated to be 4-6 h. At steady-state, significant CHF3381 plasma concentrations were detected at predose with a modest accumulation (1.3-1.5 times), showing that the drug given twice daily is active over the entire 24 h period. Plasma concentrations of CHF3567 and of 2-aminoindane were also proportional to the dose of CHF3381. CHF3381 dose-dependently inhibited MAO-A activity with peak effects at steady-state of 27 +/- 4%, 46 +/- 2% and 65 +/- 5% after 100 mg twice daily, 200 mg twice daily and 400 mg twice daily, respectively. There were no significant effects of CHF3381 on attention (rapid visual information processing), motor co-ordination (body sway) or memory (learning memory task) at any of the doses. At steady-state, there was a significant decrease in alertness (Bond & Lader visual analogue scale) in the 400 mg twice daily group compared with placebo. CONCLUSIONS: A twice daily regimen of CHF3381 appears to be adequate from a pharmacokinetic and pharmacodynamic perspective. Plasma concentrations reached with 400 mg twice daily exceeded those observed in animals receiving pharmacologically active doses in chronic pain models.

Administration, Oral↗
PubMed2003

Altered expression of NCAM in hippocampus and cortex may underlie memory and learning deficits in rats with streptozotocin-induced diabetes mellitus.

Neurological and structural changes are paralleled by cognitive deficits in diabetes mellitus. The present study was designed to evaluate the expression of neural cell adhesion molecules (NCAM) in the hippocampus, cortex and cerebellum and to examine cognitive functions in diabetic rats. Diabetes was induced in male albino rats via intraperitoneal streptozotocin injection. Learning and memory behaviors were investigated using a passive avoidance test and a spatial version of the Morris water maze test. NCAM expression was detected in the hippocampus, cortex and cerebellum by an immunoblotting method. The diabetic rats developed significant impairment in learning and memory behaviours as indicated by deficits in passive avoidance and water maze tests as compared to control rats. Expression of NCAM 180 and 120 kDa were found to be higher in hippocampus and cortex of diabetic rat brains compared to those of control, whereas expression of NCAM 140 kDa decreased in these brain regions. Our findings suggest that streptozotocin-induced diabetes impairs cognitive functions and causes an imbalance in expression of NCAM in those brain regions involved in learning and memory. Altered expression of NCAM in hippocampus may be an important cause of learning and memory deficits that occur in diabetes mellitus.

Animals↗
PubMed2004

The challenges of understanding mammalian cognition and memory-based behaviours: an interactive learning and memory systems approach.

Various research problems are presented to illustrate the utility of using the interactive multiple learning and memory systems view to better understand normal and abnormal manifestations of mammalian behaviour. Evidence for incidental learning and memory processes is presented and various implications of this work are discussed. Empirical and theoretical work directed at understanding the cognitive and non-cognitive processes associated with place learning in the water task and context conditioning during aversive events is also presented.

Amnesia, Retrograde↗
PubMed2006

Enhancement of learning and memory by a medicinal formulation, Saenhyetang, in mice.

The effects on memory and learning ability of the Korean herbal medicine, Saenhyetang (SHT), which is consisted of nine herbs, were investigated. Hot water extracts (HWE-SHT) and ethanol extracts (EE-SHT) were used for the studies. It was shown that N-methyl-d-aspartate (NMDA) receptor 2B (NR2B) was increased in the forebrains of SHT-administrated mice (HWE-SHT), leading to enhanced activation of NMDA receptors, facilitating synaptic potentiation in response to stimulation at 10-100Hz. These HWE-SHT-treated mice exhibit superior ability in learning and memory in various behavioral tasks, showing that NR2B is enhanced by HWE-SHT treatment and also is critical in gating the age-dependent threshold for plasticity and memory formation. NMDA receptor-dependent modifications, which were mediated in part by HWE-SHT administration, of synaptic efficacy, therefore, represent a mechanism for associative learning and memory. Results suggest that oriental medical enhancement of NR2B attributes such as intelligence and memory in mammals is feasible. On the other hand, to examine the effects of EE-SHT on the learning and memory in experimental mice, the passive and active avoidance responses were studied. The EE-SHT ameliorated the memory retrieval deficit induced by ethanol, but not other memory impairment in mice. EE-SHT (10, 20mg/100g, p.o.) did not affect the passive avoidance responses of normal mice in the step through and step down tests, the conditioned and unconditioned avoidance responses of normal mice in the shuttle box and lever press performance tests, and the ambulatory activity of normal mice in normal condition. However, EE-SHT was shown to significantly decrease the spontaneous motor activity during the shuttle box test, and also to prolong the sleeping time induced by pentobarbital in mice at 20mg/kg. These results suggest that EE-SHT has an ameliorating effect on memory retrieval impairment and a weak tranquilizing action.

Animals↗
PubMed2003

Rap1 couples cAMP signaling to a distinct pool of p42/44MAPK regulating excitability, synaptic plasticity, learning, and memory.

Learning-induced synaptic plasticity commonly involves the interaction between cAMP and p42/44MAPK. To investigate the role of Rap1 as a potential signaling molecule coupling cAMP and p42/44MAPK, we expressed an interfering Rap1 mutant (iRap1) in the mouse forebrain. This expression selectively decreased basal phosphorylation of a membrane-associated pool of p42/44MAPK, impaired cAMP-dependent LTP in the hippocampal Schaffer collateral pathway induced by either forskolin or theta frequency stimulation, decreased complex spike firing, and reduced the p42/44MAPK-mediated phosphorylation of the A-type potassium channel Kv4.2. These changes correlated with impaired spatial memory and context discrimination. These results indicate that Rap1 couples cAMP signaling to a selective membrane-associated pool of p42/44MAPK to control excitability of pyramidal cells, the early and late phases of LTP, and the storage of spatial memory.

Animals↗
PubMed1998

To fear or not to fear: what was the question? A potential role for Ras-GRF in memory.

Learning, making memories, and forgetting are thought to require changes in the strengths of connections between neurons. Such changes in synaptic strength occur in two phases: an early phase that is likely mediated by covalent modifications to existing proteins, and a delayed phase that depends on new gene expression and protein synthesis. However, the biochemical mechanisms by which neuronal activity leads to changes in synaptic strength are poorly understood. Recently, it has been shown that animals that lack Ras guanine nucleotide releasing factor (Ras-GRF), a Ca(2+)-dependent activator of the small GTP-binding protein, Ras, do not learn fear responses normally, although other types of learning appear normal. These animals show defects in the delayed phase of memory formation within the neuronal circuit that mediates fear conditioning. This paper suggests that Ras-GRF couples synaptic activity to the molecular mechanisms that consolidate changes in synaptic strength within specific neuronal circuits.

Amygdala↗
PubMed1989

[Disorders of learning and memory in focal cerebral tissue lesions].

Memory and learning in man depend on complex cognitive systems, and thus on efficient associative information stores in different neocortical areas of our brain. In addition, phylogenetically older, "limbic" brain structures are needed, in order to manage these huge accociative stores in our telencephalon. This "operating system" manages memory and learning capabilities considering the "milieu interne", and especially biological and individual priorities. Our contribution attempts to sketch the anatomical outlines of this limbic operating system. Two interdependent neuronal networks may be of pivotal importance: 1. a medial limbic loop with Papez circuit as the main structure, and 2. a basolateral limbic loop including the amygdala, the subcallosal area (and the septum verum?) as well as the mediodorsal thalamic nucleus. Based on the anatomical evidence of (largely) selective, i.e. focal brain lesions the likelihood for all these relay stations as memory-related structures is discussed. Our working hypothesis assumes that combined, bilateral lesions of both limbic neuronal networks make severe, global and lasting deficits in memory and learning performance fairly likely. The lesion of only one of these limbic loops seems to cause modality-specific deficits. Unilateral lesions of the retrocommissural hippocampal formation may also account for lasting amnesia.

Brain Damage, Chronic↗
PubMed1993

[Impairment of learning and memory and the accessory symptom in aged rats as senile dementia model (2)--Learning and memory].

We attempted to investigate the ability of learning and memory of aged rats. Swimming speed of aged rats in Morris's water maze was slower compared with that of young rats. Therefore, we used goal distance to indicate ability of learning and memory. In training session, distance for both groups decreased with training, but in aged rats it was significantly longer than that in young rats. In retention test 24 d after the training, distance in aged rats was longer than that in young rats, although there was no difference in distance for both groups between acquisition and retention tests. The distance in the working memory tended to increase with aging. There was no difference in time spent within platform phase in probe trial, in percent movement of first trial in habituation test, and in step-through latency in passive avoidance, between young and aged rats. Drinking latency for aged rats in water finding task was significantly longer compared with that in young rats. These findings suggest that learning and memory were impaired by aging in spatial and latent learning tasks. Aged rats could acquire and maintain memory of simple tasks, but in spatial tasks they tended to show decreased ability of retention and working memory.

Aging↗
PubMed1991

Distribution of mRNA for the calmodulin-sensitive adenylate cyclase in rat brain: expression in areas associated with learning and memory.

The Drosophila learning mutant, rutabaga, is deficient in the calmodulin-sensitive adenylate cyclase, and studies of associative learning in Aplysia have implicated this enzyme in neuroplasticity. Therefore, the distribution of mRNA encoding the calmodulin-sensitive adenylate cyclase in rat brain was examined by in situ hybridization. mRNA for this enzyme is expressed in specific areas of brain that have been implicated in learning and memory, including the neocortex, the hippocampus, and the olfactory system. The presence of mRNA for this enzyme in the pyramidal and granule cells of the hippocampal formation provides evidence that it is found in neurons. These data are consistent with the proposal that the calmodulin-sensitive adenylate cyclase plays an important role in learning and memory.

Adenylyl Cyclases↗
PubMed2005

Activity of striatal neurons reflects dynamic encoding and recoding of procedural memories.

Learning to perform a behavioural procedure as a well-ingrained habit requires extensive repetition of the behavioural sequence, and learning not to perform such behaviours is notoriously difficult. Yet regaining a habit can occur quickly, with even one or a few exposures to cues previously triggering the behaviour. To identify neural mechanisms that might underlie such learning dynamics, we made long-term recordings from multiple neurons in the sensorimotor striatum, a basal ganglia structure implicated in habit formation, in rats successively trained on a reward-based procedural task, given extinction training and then given reacquisition training. The spike activity of striatal output neurons, nodal points in cortico-basal ganglia circuits, changed markedly across multiple dimensions during each of these phases of learning. First, new patterns of task-related ensemble firing successively formed, reversed and then re-emerged. Second, task-irrelevant firing was suppressed, then rebounded, and then was suppressed again. These changing spike activity patterns were highly correlated with changes in behavioural performance. We propose that these changes in task representation in cortico-basal ganglia circuits represent neural equivalents of the explore-exploit behaviour characteristic of habit learning.

Acoustic Stimulation↗
PubMed2006

Predictive value of Wada memory scores on postoperative learning and memory abilities in patients with intractable epilepsy.

OBJECT: Surgery for refractory epilepsy often bestows significant relief but may cause memory impairment. The risk of postoperative memory loss can be determined by the intracarotid amobarbital procedure, or the Wada test. Chemical inactivation of the hemisphere on the side of the lesion is usually performed first, followed by inactivation of the contralateral hemisphere. Patients who demonstrate adequate memory capacity of the contralateral hemisphere following deactivation of the ipsilateral hemisphere are considered good candidates for anterior temporal lobectomy. Evidence for the contribution of deactivating the contralateral healthy hemisphere remains inconclusive. METHODS: The authors analyzed results in 32 patients with intractable epilepsy who had undergone a bilateral Wada test followed by an anterior temporal lobectomy and in whom the findings of both pre- and postsurgical neuropsychological evaluations were available. The Wada memory scores were correlated with the difference in scores between pre- and postsurgical standardized memory test scores. CONCLUSIONS: Analyses revealed no significant relationship between the Wada memory scores in the contralateral hemisphere and postsurgical changes in memory abilities. There was, however, a significant negative correlation between the Wada memory score in the ipsilateral hemisphere and postsurgical memory changes, particularly in patients with right hemisphere epileptogenic lesions (p = 0.0007). The results of this study are discussed vis-à-vis two theories of hippocampal function, and the authors stress the importance of the functional status of the surgical hemisphere in the prediction of postsurgical memory changes.

Adolescent↗
PubMedDate not supplied

Neuropathological studies on strains of senescence-accelerated mice (SAM) with age-related deficits in learning and memory.

In a series of inbred Senescence-Accelerated mice (SAM) strains, accelerated-senescence prone SAMP substrains show early onset and rapid advancement of senescence. SAMP8 and SAMP10, in particular, exhibit a significant age-related deterioration in memory and learning for passive and active avoidance tasks with, respectively, a low and high incidence of systemic senile amyloidosis. In the brains of both SAMP8 and SAMP10 strains, we have found numerous morphological alterations. Here we review the changes seen in both neuronal or glial components in SAMP8/P10 brains. They may serve as markers of the neuronal degeneration leading to the deficits in learning and memory.

Aging↗
PubMed2000

Beta-amyloid precursor polypeptide in SAMP8 mice affects learning and memory.

Senescence accelerated (SAMP8 [P8]) mice develop age-related deficits in memory and learning. We show that increased expression of amyloid precursor protein (APP) and its mRNA in the hippocampus are also age-related. Immunocytochemical data suggest that a critical amount of APP expression may be needed to generate amyloid (Abeta) protein plaques in the hippocampus. Deficits in acquisition and retention test performance were alleviated by administration of antibody to Abeta protein into the cerebral ventricles. This reversal of cognitive deficits provides a link between increased expression of both APP and Abeta protein and learning and memory loss in these mice.

Age Factors↗