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PubMed1993

Preferential expression in mushroom bodies of the catalytic subunit of protein kinase A and its role in learning and memory.

Involvement of the cAMP cascade in Drosophila learning and memory is suggested by the aberrant behavioral phenotypes of the mutants dunce (cAMP phosphodiesterase) and rutabaga (adenylyl cyclase). Line DCO581, isolated via an enhancer detector screen for genes preferentially expressed in the mushroom bodies, contains a transposon in the first exon of the catalytic subunit gene (DCO) of protein kinase A (PKA). RNA in situ hybridization and immunohistochemistry show that DCO is preferentially expressed in the mushroom bodies. The DCO581 insertion and an independently isolated hypomorphic allele (DCOB10) each produce homozygous lethality and a 40% decrease in PKA activity in heterozygotes. This decrease has mild effects on learning but no effect on memory. However, the 80% reduction in activity obtained by constructing heteroallelic yet viable DCO581/DCOB10 animals results in a dramatic learning and memory deficit. These results suggest that PKA plays a crucial role in the cAMP cascade in mushroom bodies to mediate learning and memory processes.

Animals↗
PubMed1979

Effects on learning and memory of 2-week treatments with chlordiazepoxide lactam, N-desmethyldiazepam, oxazepam and methyloxazepam, alone or in combination with alcohol.

A double-blind study with 40 healthy students was done in order to measure the effects of a 2-week treatment with chloridiazepoxide lactam (5 mg), nordiazepam (10 mg), oxazepam (15 mg) and methyloxazepam (20 mg) on immediate memory and associative learning. The drugs were administered t.i.d. and the tests were done after the very last capsule was given. It was ingested with a placebo drink and 0.5 g alcohol/kg body weight. Oxazepam and methyloxazepam alone behaved similar to the placebo. Immediate memory was significantly impaired following the treatment with nordiazepam, chlordiazepoxide lactam, alcohol, and after the simultaneous administration of nordiazepam and chlordiazepoxide lactam with alcohol. Chlordiazepoxide lactam was the only drug which alone impaired associative learning. Also alcohol alone, and all the drugs in combination with alcohol retarded learning acquisition.

Adult↗
PubMed2003

Implicit learning in memory rehabilitation: a meta-analysis on errorless learning and vanishing cues methods.

The objective of this study was to present a quantitative review on the treatment effects of memory rehabilitation techniques based on intact implicit learning capacity in amnesic patients, that is, errorless learning and the method of vanishing cues. English-language journal articles focusing on these rehabilitation techniques were examined using MedLine (1966-2002) or PsychInfo (1887-2002), as well as additional papers listed in the references of these articles. Studies had to meet the following inclusion criteria: (1) original data were reported, (2) memory rehabilitation was studied in memory-impaired patients, (3) a control intervention was included, (4) exact scores were listed for both intervention conditions, or the exact statistics were presented. Studies were classified on the basis of the to-be-learned material and the method of intervention (errorless learning, vanishing cues, control intervention), patient characteristics were determined, and the tasks that were used were taken into account. Effect sizes and variances were computed for each individual study compared to control treatment using within-group statistics. A "large" and statistically significant ES was found for errorless learning treatment, but no significant ES was demonstrated for the vanishing cues method. The results of the present study show that the errorless learning technique is effective in amnesic patients. The effects on the vanishing cues method are only small (and nonsignificant).

Adult↗
PubMed1995

The nature of learning and memory impairments in schizophrenia.

The California Verbal Learning Test was used to characterize the learning and memory impairment in schizophrenia (SC) and to evaluate potential clinical and demographic factors associated with this impairment. SC patients (n = 175) performed worse than normal comparison (NC) subjects (n = 229) on all learning, recall, and recognition memory measures. The most important clinical correlates of these impairments were earlier age of onset, more negative symptoms, and greater anticholinergic medication dosage. SC patients showed a prominent retrieval deficit as indicated by disproportionate improvement when tested in a recognition, rather than a free recall, format. A residual impairment seen with recognition testing suggests a mild encoding deficit as well. In contrast, the relative absence of a storage deficit is suggested by the lack of rapid forgetting. Using a discriminant function analysis that differentiates cortical dementia [i.e., Alzheimer's disease (AD)], subcortical dementia [i.e., Huntington's disease (HD)], and normals, it was found that 50% of the SC patients were classified as having a subcortical memory profile and 35% were classified as having a normal profile, whereas only 15% were classified as having a cortical memory profile. Although these findings reflect the clinical heterogeneity often found in SC, results suggest that most SC patients demonstrate a pattern of learning and memory impairments that resembles the pattern seen in patients with primary subcortical (specifically striatal) pathology.

Adult↗
PubMed1994

The behavioral neurobiology of learning and memory: a conceptual reorientation.

Research on the neurobiology of learning and memory has been guided by two major theories: (i) memory as a psychological process and (ii) memory as a change in synaptic neural connectivity. It is not widely recognised that not only are these theories different but, moreover, they are fundamentally incompatible. Confusion concerning basic concepts in the learning and memory field in mammals has lead to the creation of an extensive but often inconclusive experimental literature. However, one important conclusion suggested by recent work in this field is that experience-dependent changes in neural connectivity occur in many different brain systems. Particular brain structures, such as the hippocampus, do not play any uniquely important role in experience-dependent behavior. Research in learning and memory can be best pursued on the basis of biological studies of animal behavior and a cellular approach to brain function.

Animals↗
PubMed2002

Strain differences in activity and emotionality do not account for differences in learning and memory performance between C57BL/6 and DBA/2 mice.

This study examined emotionality, activity, learning and memory, as well as the influence of emotionality and activity on learning and memory performance in C57BL/6 and DBA/2 mice using a mouse-test battery. DBA/2 mice performed more poorly than C57BL/6 mice in complex learning tasks such as the water maze and object recognition tasks. In contrast, C57BL/ 6 mice showed attenuated habituation tonovelty in the open field apparatus and poorer performance in the step-down passive avoidance task. The C57BL/6 mice were less exploratory and more anxious than the DBA/ 2 mice. The anxiety score (open arm entries in the elevated plus maze) was significantly correlated with all measures of learning and memory in the object recognition task, and some measures in the passive avoidance and water maze tasks. Analysis of covariance (with open arm entries as a covariate) revealed that some measures on trial 1 of the object recognition task, but not the memory scores on trial 2,were confounded by anxiety. No confounding factors of anxiety were found in the water maze or passive avoidance tasks. Similar results were obtained with the activity scores (line crossing and rearing in the open field). In conclusion, strain differences in activity and anxiety did not account for strain differences in learning and memory performance of C57BL/6 and DBA/2 mice. Nonetheless, the importance of using complete behavioural test batteries should be stressed to ensure that strain differences in learning and memory tasks are not confounded by non-cognitive factors.

Animals↗
PubMed2003

Mice lacking Tropomodulin-2 show enhanced long-term potentiation, hyperactivity, and deficits in learning and memory.

Actin filaments control cell morphology and are essential to the growth of dendritic spines and the plasticity of hippocampal long-term potentiation (LTP). The length of these filaments is regulated in muscle and nonmuscle cell types by tropomodulins 1-4 (Tmod1-4), a family of proteins that cap the pointed ends of actin filaments. To investigate whether tropomodulins could play a role in synaptic plasticity, learning, memory, or behavior, we created mice lacking Tropomodulin-2 (Tmod2), which is highly expressed in neuronal structures. Tmod2(lacZ-/-) mice are viable and fertile and exhibit no gross morphological or anatomical abnormalities, but behavioral analysis found hyperactivity, reduced sensorimotor gating, and impaired learning and memory. Electrophysiological analysis revealed enhanced LTP in Tmod2(lacZ-/-) mice. These studies suggest that Tmod2 plays a role in behavior, learning, memory, and synaptic plasticity.

Animals↗
PubMed1983

Learning and memory impairment in adult rats due to severe zinc deficiency during lactation.

In a series of three experiments, adult rats who suffered severe zinc deficiency and/or undernutrition during lactation were tested in a 17-arm radial maze for working memory, reference memory, forgetting and learning. In Experiment 1, eight out of 17 arms were baited. The zinc deficient (ZD) and undernourished (PF) rats revealed a learning deficit when compared to adequately nourished rats (AL). ZD rats also appeared to display a loss of working memory. No evidence of loss of reference memory was observed among any of the groups. A reverse learning procedure was used in Experiment 2 to test the same rats used in Experiment 1. ZD rats were significantly inferior in performance of the reverse learning task compared to the AL and PF rats. No significant differences in performance were noted between the AL and PF rats. Although all groups displayed forgetfulness from Experiment 1 to Experiment 2, no significant differences in forgetfulness were evidenced among the groups. In Experiment 3, all 17 arms were baited. The ZD rats displayed a significant working memory deficit as compared to the AL and PF rats. No significant differences in working memory between the AL and PF rats occurred. The possibility that the differences in performance were due to differences in food motivation or attention was considered and rejected. It was concluded that ZD rats experienced a severe learning deficit and some working memory deficit while the PF rats experienced a mild learning deficit as compared to the AL rats.

Animals↗
PubMed1997

Gene targeting and the biology of learning and memory.

The general goal of genetic studies of learning and memory is to develop and test theories that explain the animal's behavior in neuroanatomical, neurophysiological, cellular, and molecular terms. In this review we describe the role that gene targeting and other transgenic techniques have had in the study of mammalian learning and memory. We focus especially on the hippocampus, a brain structure that is thought to be central to the processing and temporary storage of complex information. We also discuss the main issues that confront this young field, as well as our vision for its future.

Animals↗
PubMed1996

Phenobarbital in the anticonvulsant dose range does not impair learning and memory or alter brain AChE activity or monoamine levels.

The learning and memory in adult, male Wistar rats were assessed using the T-maze and passive avoidance tests after chronic administration of phenobarbital (PB) at 5, 15, 30, 60, or 75 mg/kg intraperitoneally (IP) for 21 days. The PB levels in plasma, the acetylcholine esterase (AChE) activity in the motor cortex, pyriform cortex, olfactory bulb, striatum, septum, and hippocampus and the levels of serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), dopamine (DA), dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA) levels in the hippocampus were measured. There was no significant change in learning and memory, AChE activity, or monoamine levels at plasma PB levels of 1.5, 6.0, 9.0, and 25 micrograms/ml (corresponding to doses of 5, 15, 30, or 60 mg/kg PB, respectively). However, at a plasma level of 55 micrograms/ml (75 mg/kg), PB caused impairment in learning and memory. It was associated with an increase in AChE activity and 5-HT levels in the hippocampus. The results indicate that chronic PB administration may not be linked to impaired learning and memory functions at doses used in anticonvulsant therapy.

Acetylcholinesterase↗
PubMed2005

Executive control of learning and memory in children with bilateral spastic cerebral palsy.

Executive control of learning and memory was examined in children with bilateral spastic cerebral palsy (SCP). We hypothesized that SCP-related brain damage would disrupt executive but not associative aspects of learning and memory. To test this hypothesis, the California Verbal Learning Test-Children's Version was administered to 16 children with bilateral SCP and 19 control children ranging from 6 to 18 years of age. Controlling for general verbal ability, the groups did not differ in initial learning and retention of information over time, suggesting that associative learning and memory processes subserved by medial temporal brain regions were relatively intact in children with SCP. In contrast, impairments in learning over repeated trials, strategic processing, and inhibition in the SCP group pointed to disruptions in prefrontally-mediated executive aspects of learning and memory. The inhibitory deficit was more pronounced in younger children with SCP, suggesting a developmental delay in this ability.

Adolescent↗
PubMed2004

Early administration of nicotinamide prevents learning and memory impairment in mice induced by 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine.

BACKGROUND AND PURPOSE: NAD has been reported to improve the dementia of the Alzheimer type or sensory register, short- and long-term memory loss in the aged. Although nicotinamide has been confirmed to decrease infarct volumes and neurological deficit findings in several animal stroke models, it is not clear whether its neuroprotective effects can prevent memory damage sequelae. METHODS: We have addressed this topic by designing two behavioral paradigms. A memory impairment and cognitive change model was used in mice following 1-methyl-4-phenyl-l, 2, 3, 6-tetrahydropyridine (MPTP) exposure. Step-down and step-through tests were performed to examine the effects of nicotinamide on learning and memory impairment. RESULTS: It was found that the early administration of nicotinamide (2 h after the injection of MPTP) could decrease error numbers, lessen stimulation time and prolong residence duration on the safety platform in the step-down test. Delayed administration of nicotinamide resulted in decreased effects. Similar results were found in the step-through test. Nicotinamide administrated 12 h after the induction of a memory-impairment model still exerted its effects on memory dysfunction. CONCLUSIONS: The injection of MPTP can cause a loss of brain functions including learning and memory. Learning and memory dysfunction probably occurs secondary to damage to arterioles and dopaminergic neurons by MPTP. By inhibiting oxidative stress, increasing NAD synthesis and ATP production and inhibiting poly (ADP-ribose) polymerase, nicotinamide is known to rescue the still viable, but injured, cells. This rescue process may partially restore learning and memory.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1978

[Effect of right-sided hippocampotomy on memory and learning ability].

The authors report the results of memory and learning ability investigations in a patient treated with hippocampotomy (uncotomy) for severe epileptic seizures. In the seeg investigations the changes were most pronounced in the hippocampus. In psychological investigations before the operation deep disturbances of verbal memory with unchanged (normal) level of mental efficiency were found. After stereotaxic treatment epileptic seizures disappeared completely, the patient completed a vocational school and started working. Follow up examinations during 6 years after the operation failed to demonstrate any decrease in mental efficiency. The impairment of verbal memory and learning ability was decreased significantly.

Child↗
PubMed1999

Chronic administration of docosahexaenoic acid improves reference memory-related learning ability in young rats.

Wistar rats were fed a fish oil-deficient diet through three generations. The young (five-week-old) male rats of the third generation were randomly divided into two groups. Over 10 weeks, one group was perorally administered docosahexaenoic acid dissolved in 5% gum Arabic solution at 300 mg/kg/day; the other group received a similar volume of vehicle alone. Five weeks after starting the administration, the rats were tested for learning ability related to two types of memory, reference memory and working memory, with the partially (four of eight) baited eight-arm radial maze. Reference memory is information that should be retained until the next trial. Working memory is information that disappears in a short time. Entries into unbaited arms and repeated entries into visited arms were defined as reference memory errors and working memory errors, respectively. Docosahexaenoic acid administration over 10 weeks significantly reduced the number of reference memory errors, without affecting the number of working memory errors, and significantly increased the docosahexaenoic acid content and the docosahexaenoic acid/arachidonic acid ratio in both the hippocampus and the cerebral cortex. In addition, the ratio demonstrated a significantly negative correlation with the number of reference memory errors. These results suggest that chronic administration of docosahexaenoic acid is conducive to the improvement of reference memory-related learning ability, and that the docosahexaenoic acid/arachidonic acid ratio in the hippocampus or the cerebral cortex, or both, may be an indicator of learning ability.

Animals↗
PubMedDate not supplied

The effects of acetyl-l-carnitine on experimental models of learning and memory deficits in the old rat.

Experimental models of learning and memory deficits in aged rats can be studied by means of behavioural tests that provide an important tool for evaluating the effect of drugs on these parameters. Active and passive avoidance tests showed a clear impairment of learning and memory capacity of old rats. These tests were also used to study the behavioural effect of acetyl-l-carnitine in aged rats. The subchronic treatment with this drug was followed by a significant improvement of acquisition and retention of avoidance responses, indicating a facilitation of learning and memory capacity of aged rats.

Acetylcarnitine↗
PubMed1998

Roles of kappa-opioid receptor agonists in learning and memory impairment in animal models.

The role of kappa-opioid receptor agonists on learning and memory is controversial. In this review, the effects of dynorphin A (1-13) and U-50,488H on learning and memory impairments in mice and rats are summarized. Muscarinic cholinergic antagonists and a nicotinic cholinergic antagonist significantly impaired learning and memory in various behavioral tests. Administration of dynorphin A (1-13) or U-50,488H reversed the impairment of learning and memory. U-50,488H completely blocked the decrease in acetylcholine release induced by mecamylamine, while it only partially blocked the increase of acetylcholine induced by scopolamine. The antagonistic effect of U-50,488H was abolished by pretreatment with nor-binaltorphimine, a selective kappa-opioid receptor antagonist. Dynorphin A (1-13) and U-50,488H did not affect the impairment of learning and memory induced by the blockade of NMDA-receptors by dizocilpine ((+)-MK-801. These results suggest that kappa-opioid receptor antagonist reverses the impairment of learning and memory induced by the blockade of cholinergic transmission and abolishes the decrease of acetylcholine release via the kappa-opioid receptor-mediated neuronal system.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed2006

[Effects of early intervention on learning and memory in young rats of marginal vitamin A deficiency and it's mechanism].

OBJECTIVE: In recent years, some experiments on vitamin A-deprived animals reveal a progressive and ultimately profound impairment of hippocampal CA1 area's long-term potentiation and these losses are fully reversible by dietary vitamin A replenishment in vivo. Our previous study revealed that marginal vitamin A deficiency (MVAD) beginning from embryonic period impairs learning, memory and long-term potentiation (LTP) in young rats. But the losses might not be reversible if the vitamin A supplementation is late, especially when the critical period of hippocampus development is missed. The present study aimed to observe the recovery of learning and memory in vitamin A marginally deficient young rats after early intervention with vitamin A supplementation and begin to study the mechanism. METHODS: Rats were divided into control, MVAD, vitamin A intervention 1 (VAI1) and VAI2 groups in this study. In control group (10 young rats) the dams and pups were fed with normal diet (VA 6500 U/kg). In MVAD group (19 young rats) the dams and pups were fed with MVAD diet (VA 400 U/kg). In VAI1 group (10 young rats) the dams were fed with MVAD diet till day 14 of pregnancy, then were fed with normal diet and the pups were fed with normal diet. In VAI2 group (13 young rats) the dams were fed with MVAD diet till delivery, then were fed with normal diet and the pups were fed with normal diet too. All the young rats were killed at the age of 7 weeks. During the last week of the experiment, the shuttle box active avoidance reaction tests were carried out. At week 7, the hippocampal CA1 LTP was detected by electrophysiological technique. The expression of RAR-alpha, RAR-beta, RXR-beta, RXR-gamma, RC3 and tTG mRNA was detected by using semi-quantified RT-PCR in hippocampus. RESULTS: (1) The times to reach the learning standard in MVAD group (45.6 +/- 12.1) were more than those in control group (17.1 +/- 4.4) (P < 0.01), in both VAI1 group (20.8 +/- 3.1) and VAI2 group (22.1 +/- 4.0) were more than those in group MVAD (P < 0.01), and there were no significant differences among groups VAI1, VAI2 and control (P > 0.05) in active avoidance reaction tests. (2) The changes of field excitatory postsynaptic potentials (fEPSP) slope for MVAD group [(22.9 +/- 9.4)%] and VAI2 group [(39.1 +/- 4.33)%] were less than that of control group [(57.5 +/- 27.3)%], respectively (P < 0.05). No significant difference was found between VAI1 and control group (P > 0.05). (3) The expression of RAR-beta and RXR-beta mRNA decreased by 48.72% and 37.84% respectively (P < 0.05) compared with control, but the expression of RAR-beta mRNA in group VAI1 was higher than that in group MVAD (P = 0.065). The expression of RC3 mRNA in MVAD group was lower than that in control (P = 0.061) and RAR-alpha mRNA in MVAD group was higher than that in control (P = 0.061). The expression of RXR-gamma and tTG mRNA had no significant difference among different groups as determined with semi-quantified RT-PCR in hippocampus. CONCLUSION: Early vitamin A intervention may make the impaired learning and memory behavior due to marginal vitamin A deficiency recover to the normal level in young rats, but lip losses in group VAI2 might not be reversible. Vitamin A may modulate the expression of RC3 mRNA by affecting RAR-alpha, RAR-beta and RXR-beta to influence the LTP, learning and memory.

Animal Nutritional Physiological Phenomena↗
PubMed2001

Characterization of microsphere embolism-induced impairment of learning and memory function and the cholinergic system.

The impairments of learning and memory function and of the cholinergic system were examined in rats with microsphere embolism. Microsphere embolism was induced by injection of 900 microspheres with a diameter of 48 microm into the right internal carotid artery. The retention latency of a passive avoidance test was shortened and the escape latency of a water maze test was prolonged, when the animals were tested on the 5th to 10th day after the embolism, suggesting learning and memory dysfunction. Cholinergic parameters of the striatum and hippocampus, such as acetylcholine (ACh) content (67 and 60% decrease, respectively), choline acetyltransferase (ChAT) activity (45 and 56% decrease, respectively), and Bmax of muscarinic acetylcholine M1-receptor (43 and 37% decrease, respectively), were reduced on the 11th day after the embolism, suggesting attenuation of ACh synthesis and a decrease in the number of muscarinic acetylcholine M1-receptors mainly in the striatum and hippocampus. Areas not stained with triphenyltetrazolium chloride, an indication of infarction, were detected mainly in the striatum and hippocampus and partly in the frontal cortex on the 11th day after the embolism. The results suggest that an animal with microsphere embolism may be a good ischemic model with relatively sustained impairments of learning and memory function and of the striatal and hippocampal cholinergic system.

Animals↗