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PubMedDate not supplied

Classical conditioning: the Rosetta stone for brain substrates of age-related deficits in learning and memory.

The three chapters on the use of classical conditioning paradigms to investigate neurobiological and behavioral substrates of memory impairments with aging are in close agreement on all key issues. Based on these chapters, it is argued here that classical conditioning of discrete behavioral responses in rabbit and other mammals is among the most promising animal models of the human condition in which to analyze brain mechanisms of normally occurring age-related deficits in learning and memory.

Aging↗
PubMed2004

Role of hippocampal CA3 mu-opioid receptors in spatial learning and memory.

The dorsal CA3 region of the hippocampus is unique in its connectivity, sensitivity to neurotoxic lesions, and its ability to encode and retrieve episodic memories. Computational models of the CA3 region predict that blocking mossy-fiber and/or perforant path activity to CA3 would cause impairments in learning and recall of spatial memory, respectively. Because the CA3 region contains micro-opioid receptors and receives inputs from the mossy-fiber and lateral perforant pathways, both of which contain and release opioid peptides, we tested the hypothesis that inactivating micro-opioid receptors in the CA3 region would cause spatial learning and memory impairments and retrieval deficits. In this study, male Sprague Dawley rats were trained in a Morris water maze after a single bilateral intrahippocampal injection of either saline or the selective and irreversible micro-opioid receptor antagonist beta-funaltrexamine (beta-FNA) into area CA3. We found that micro-opioid receptor binding decreased 24 hr after beta-FNA injection and returned to control levels 11 d after injection. Injections of beta-FNA into the CA3 region, but not into the ventricles, caused a significant impairment in the acquisition of spatial learning without causing sensory or motor deficits. New learning was not affected once micro-opioid receptor levels replenished (>11 d after injection). In pretrained animals, beta-FNA significantly impaired spatial memory retrieval and new (reversal) learning. These data are consistent with theoretical models of CA3 function and suggest that CA3 micro-opioid receptors play an important role in the acquisition and retrieval of spatial memory.

Animals↗
PubMed2005

Melatonin improves learning and memory performances impaired by hyperhomocysteinemia in rats.

Oxidative stress has been proposed as a possible mechanism underlying many neurodegenerative diseases associated with hyperhomocysteinemia. In the present study, we investigated the possible link between oxidative stress, expression of neural cell adhesion molecules and spatial learning deficits induced by chronic hyperhomocysteinemia. Furthermore, the effectiveness of antioxidant melatonin against homocysteine neurotoxicity was also examined. Male Wistar rats were treated with either saline or methionine to induce hyperhomocysteinemia and half of methionine-treated rats administered daily melatonin in a dose of 10 mg/kg. We observed that chronic administration of melatonin significantly reduced the lipid peroxidation and restored the decreased glutathione levels induced by chronic hyperhomocysteinemia. Chronic hyperhomocysteinemia significantly impaired learning and memory performance in the passive avoidance test and Morris water maze task. We also found that these cognitive deficits were reversed by chronic treatment with antioxidant melatonin. Furthermore, melatonin administration was able to modulate the expression pattern of neural cell adhesion molecules in hippocampus. The results provide evidence that homocysteine induces long-lasting behavioral deficits, which are possibly caused by oxygen reactive species generation, and by changing in synaptic plasticity and also suggest that melatonin treatment has the ability to prevent nervous system against homocysteine toxicity.

Analysis of Variance↗
PubMed2004

Learning and memory impairment in rats with chronic atypical absence seizures.

Atypical absence seizures (AASs) represent a pediatric malignant seizure type that commonly exists as a component of Lennox-Gastaut syndrome. AAS involves both the hippocampal and thalamocortical circuitry in slow spike-and-wave discharges (SSWD) and is associated with cognitive dysfunction. The electrographic, behavioral, and pharmacological features of clinical AAS have been reproduced in rats chronically in the AY-9944 (AY) model. AY rats show spontaneous SSWD involving the hippocampus, a structure that is highly implicated in learning and memory. The purpose of the present study was to determine whether AY rats exhibit cognitive deficits that mirror those observed in AAS clinically. Hippocampal function was examined in AY animals both in vitro with electrophysiology (i.e., synaptic plasticity) and in vivo with a hippocampus-dependent radial arm maze (RAM) task that is designed to assess spatial cognition. In vitro tests of synaptic plasticity revealed impairments in long-term potentiation (LTP), paired-pulse facilitation (PPF), and presynaptic depression (PD). Consistently, performance of AY animals in RAM revealed fewer perfect entries, a greater number of errors, and required more training days to learn the task than saline-treated controls. The abolishment of spontaneous seizures by ethosuximide failed to recover the perturbed spatial learning and working memory in AY animals. AY rats demonstrate altered hippocampal functioning as manifested by altered synaptic plasticity and cognition. The relationship between AAS and cognitive deficit remains uncertain and the pathophysiology of both in AY treated requires further investigation.

Animals↗
PubMed2000

Bedside evaluation of learning and memory: descriptive information on a shortened version of the Luria Memory Words Test.

Descriptive information on the shortened version of the Luria Memory Words Test (LMWT-SF), a serial word-learning list of seven items, administered across five trials with a three-minute delay, is presented. The purpose of the investigation was to determine what constituted adequate performance among nondemented elderly inpatients, and to compare the results to traditional bedside memory measures among elders diagnosed with dementia. Results revealed significant group differences on Trials 3, 4, 5, total learning score, and the delay trial among demented and non-demented geriatric inpatients. Sensitivity and specificity ratings for the LMWT-SF delay trial were 80% and 72%, respectively, at a cut-off of 3 / 4, and 71% and 60%, respectively, for the total learning score, at a cut-off of 26 / 27. While this measure cannot take the place of a comprehensive evaluation of memory and learning, LMWT-SF performance can suggest when a more comprehensive evaluation is required, and may provide value as a cost-effective screening tool.

Aged↗
PubMed1999

Learning and memory in the FMR1 knockout mouse.

The fragile X [fra(X)] syndrome is manifested phenotypically as a developmental disability comprised mainly of moderate-to-severe mental retardation (MR). Deficits are especially evident in auditory and visual short-term memory. Recently, an FMR1 knockout mouse developed by the Dutch-Belgian Fragile X Consortium demonstrated significantly lower visual-spatial abilities than littermate controls. We wondered if these results were associated with learning per se or to performance deficits only. Thus, we examined learning and memory in male FMR1 knockout mice crossbred from Fvb and E129 strains, and in male Fvb control mice, using operant conditioning techniques. In Experiment 1, we demonstrated that two aged male FMR1 knockouts could acquire the necessary bar-press response to discriminate visual (L+) and auditory (N+) stimuli. In Experiment 2, we showed that three naive male knockouts and two naive male controls, all 12 weeks old, also learned to discriminate L+ and N+. A third component, a complex discrimination task, during which light and noise were presented concurrently without reinforcement (LN-) was added to each session. All knockouts acquired both L+ and N+ discriminative responses in fewer sessions and with higher discrimination ratios than either control. Moreover, all knockouts exhibited the typical response pattern associated with complex discrimination (LN-) tasks. However, neither control made the complex discrimination. Our findings were unexpected and raise issues concerning FMR1 mouse strains and their cognitive-behavioral testing.

Animals↗
PubMed1997

[Effects of zinc deficiency in fodder on brain development, learning and memory in rats].

Zinc deficiency (ZD) model was established in young rats starting from their lactation period. Effects of ZD in fodder on brain development and learning and memory were observed with electron microscopy and neurobiochemical and electroneurophysiological methods, and its mechanism was studied. Results showed that 1. brain weight, hippocampal weight, and serum and hippocampal zinc concentrations were significantly lower in ZD group than those in controls; 2. proportion of induced long-term potentiation (LTP) was zero in ZD group and proportion of active avoidance response decreased profoundly in ZD group, significantly lower than that in normal controls whose LTP proportion was 100%; 3. concentrations of excitatory and inhibitory amino acids, glutamic acid, gamma-aminobutyric acid in cerebral cortex and hippocampus and nitrous oxide in hippocampus were significantly higher in ZD group than those in normal one, and content of somatostatin in hippocampus and DNA in pyramidocytes were significantly lower in ZD group than those in normal one; and 4. number of synaptic vesicles in pyramidocytes of hippocampus decreased obviously in ZD group. It suggests that brain development and function are obviously affected by fodder zinc deficiency in rats.

Animals↗
PubMed2005

Galanin impairs performance on learning and memory tasks: findings from galanin transgenic and GAL-R1 knockout mice.

Galanin (GAL) impairs performance on cognitive tasks when administered centrally to rats. GAL transgenic (GAL-tg) mice overexpressing endogenous GAL show deficits on the probe trial of the Morris water maze spatial learning task, on the social transmission of food preference olfactory memory task, and on the trace cued fear conditioning emotional learning and memory task. Knockout mice deficient in the GAL-R1 receptor subtype were normal on most memory tasks, while showing a small deficit in trace cued fear conditioning, suggesting a selective role for the GAL-R1 in aversive memories, and implicating other GAL receptor subtypes in spatial learning and olfactory social memory. The growing body of rodent literature implicating excess GAL in cognitive impairment is relevant to the overexpression of GAL in the basal forebrain during the progression of Alzheimer's disease.

Animals↗
PubMed1994

Explicit memory, procedural learning and lexical priming in Alzheimer's disease.

Different aspects of memory functions were studied in two groups of patients with Alzheimer's disease (AD) and in normal elderly controls. The tests included: explicit memory tests with free and cued recall, and recognition measures; learning of a motor skill; learning of a perceptual skill with verbal material; a priming task with the word stem completion paradigm. The data confirmed that, besides severe impairment for all measures of explicit memory, AD patients were able to learn and retain normally a motor skill in the rotor pursuit task, even across a long retention interval. Moreover, sparing of procedural learning was not restricted to motor tasks, since patients learned normally a mirror-reading task, demonstrating (a) rapid acquisition of the procedure, and (b) acquisition of item-specific information for repeated words. This last effect is accounted for in terms of repetition priming effects rather than of explicit memory strategies, since patients had also normal repetition effect in the word stem completion paradigm.

Aged↗