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PubMed1998

Continuous blockade of brain glucocorticoid receptors facilitates spatial learning and memory in rats.

Previously, a corticosterone surge associated with a learning task was shown to facilitate cognitive processes through brain glucocorticoid receptors (GR) while chronic overexposure to this stress hormone impaired cognition. In the present study we tested the hypothesis that opposing effects on learning and memory might also occur after either phasic or continuous blockade of brain GR by intracerebroventricular (i.c.v.) administration of the GR antagonist RU38486 (aGR). We used a Morris water maze procedure to assess spatial learning and memory abilities in male Wistar rats. The effect of phasic brain GR blockade was studied following daily pretraining administration of 10 and 100 ng/microL aGR i.c.v. on 3 consecutive days. This repetitive aGR treatment impaired spatial learning and memory dose-dependently in comparison with vehicle controls. For continuous brain GR blockade, animals received an i.c.v., infusion of aGR (10 and 100 ng/0.5 microL per h or vehicle) over 10 days. Infusion of 100 ng aGR per hour resulted in a long-lasting facilitation of spatial performance. The 10 ng aGR infusion also caused initially a facilitating effect, which was, however, transient and performance became impaired during retest. Possible anxiolytic properties of the drugs were excluded in view of the animals' behaviour in the elevated plus maze. Both doses of aGR infusion reduced the number of mineralocorticoid receptors in the hippocampus, but only the high dose of aGR resulted in a significant reduction of available GR sites. In conclusion, continuous administration of GR antagonist improves cognitive function, while phasic blockade of brain GR function causes a cognitive deficit.

Adrenocorticotropic Hormone↗
PubMed2000

[Influence of stress on learning and memory].

This paper describes the influence of stress on learning and memory. The mice receiving inescapable electroshock fail to perform the active conditioned avoidance response of lever-pressing. This is called learned helplessness, which is ameliorated by treatment with antidepressants including one of the selective serotonin reuptake inhibitors (SSRIs). It is of particular interest that posttraumatic stress disease (PTSD) accompanied by memory impairment could be improved by treatment with SSRIs. The different kinds of stress including ischemia, footshock, psychological stress, and forced swimming influence learning and memory as indexed by spontaneous alternation performance as well as passive avoidance learning. In addition, a variety of stresses influence the activity of hormones and neurotransmitters like monoamines, neuropeptides, and excitatory amino acids resulting in changes in learning and memory. Finally, the accumulation of data is necessary to clarify the exact mechanism of stress on learning and memory.

Animals↗
PubMed2004

Induced depressive behavior impairs learning and memory in rats.

While it is generally accepted that cognitive processes such as learning and memory are affected by emotion, the impact of depression on learning and memory has rarely been directly studied in experimental animals. Effects of induced depressive behavior on learning and memory were determined in rats, using an open space swim test, a novel animal model of depressive behavior that is developed recently in our laboratory. The model indexes searching activity of the animals, with the induced depressive immobility behavior showing specific sensitivity to three major prototypic classes of antidepressants and a selective serotonin reuptake inhibitor. The induced depressive behavior in rats showed a delayed response to chronic antidepressant treatment and had a lasting effect on the ability of rats to learn and recall the learned experience. It impaired the subsequent ability of rats to learn and recall both a spatial water maze task and a multi-trial passive avoidance task. These impairments were all sensitive to antidepressant therapeutics, but not to buspirone, an anxiolytic. By way of contrast, the ability of the rats to sense and move to a visible platform and to escape from an unconditioned shock stimulus was neither impaired by inducing the depressive behavior nor altered by the drug treatment, suggesting that non-specific changes in sensorimotor ability were not involved. These impairments of learning and memory indicate that the depressive behavior-induced deficits show generalizability and are not context-limited. This animal model of depressive behavior shows promising potential as a screen for novel antidepressive therapeutics and as a disease model for revealing network/cellular/molecular mechanisms in the pathophysiology of depression and depression-induced cognitive deficits.

Animals↗
PubMed2006

Standardized assessment of cognitive functioning during development and aging using an automated touchscreen battery.

This study examined the effects of age, gender and education on subjects spanning nine decades on a new cognitive battery of 12 tests. One thousand and seven participants between 6 and 82 completed the battery under standardized conditions using an automated, computerized touchscreen. Sensitive indicators of change were obtained on measures of attention and working memory, learning and memory retrieval, and language, visuospatial function, sensori-motor and executive function. Improvement tended to occur through to the third and fourth decade of life, followed by gradual decrement and/or stabilized performance thereafter. Gender differences were obtained on measures of sustained attention, verbal learning and memory, visuospatial processing and dexterity. Years of education in adults was reflected in performance on measures of verbal function. Overall, the test battery provided sensitive indicators on a range of cognitive functions suitable for the assessment of abnormal cognition, the evaluation of treatment effects and for longitudinal case management.

Adolescent↗
PubMed1995

Larger nondeclarative than declarative deficits in learning and memory in human aging.

This study used classical conditioning as a measure of nondeclarative learning and compared it with verbal learning as a declarative measure. Eighty participants were tested using 1 of 2 paradigms (400-ms and 750-ms delay) for eyeblink classical conditioning (EBCC) and the California Verbal Learning Test (CVLT). Large age differences were observed in the nondeclarative EBCC task, even in the 750-ms paradigm, which is more optimal for older adults. Age differences in the nondeclarative EBCC task were larger in the 400-ms paradigm and equal in the 750-ms paradigm to the magnitude of age differences in the declarative CVLT task. Partial correlations (removing the variance that was due to age) showed no relation between performance on the nondeclarative and declarative tasks. The results contradict the common assumption that, in the same participants, nondeclarative learning and memory are more resistant to the effects of aging than are declarative learning and memory and suggest that nondeclarative learning and memory are not unitary.

Adolescent↗
PubMed1988

Molecular approaches to learning and memory.

We are now at the stage of neurophysiology where learning and memory can be subjects of studies at a strictly molecular level, on the basis of the well-established finding that these higher nervous activities are sustained by, and formed in, the physicochemical events of specified neural mechanisms in the brain. As for the neurophysiological process of memory, much evidence has shown that short-term memory and long-term memory probably result from different molecular events in the brain, i.e., the former from reversible chemical modification of the synapses concerned, and the latter from reorganization of the synapses following synthesis of protein and its axonal transport, which causes the enduring consolidation of memories. How does the experience of individual organisms trigger the protein synthesis in the brain required for long-term memory? What is the role of protein molecules thus formed? What is the mechanism for the regulation of gene expression in the reorganization of neuronal circuits? Many such difficult problems need to be solved. Recently, cholinergic and glutamatergic neuron networks have attracted much attention because there is a strong possibility that they play a critical role in memory. The clinical implication of these findings in human memory deficit, as exemplified in senile dementia, further emphasizes the importance of neurobiological elucidation of the molecular mechanism for learning and memory.

Animals↗
PubMedDate not supplied

Using pavlovian higher-order conditioning paradigms to investigate the neural substrates of emotional learning and memory.

In first-order Pavlovian conditioning, learning is acquired by pairing a conditioned stimulus (CS) with an intrinsically motivating unconditioned stimulus (US; e.g., food or shock). In higher-order Pavlovian conditioning (sensory preconditioning and second-order conditioning), the CS is paired with a stimulus that has motivational value that is acquired rather than intrinsic. This review describes some of the ways higher-order conditioning paradigms can be used to elucidate substrates of learning and memory, primarily focusing on fear conditioning. First-order conditioning, second-order conditioning, and sensory preconditioning allow for the controlled demonstration of three distinct forms of memory, the neural substrates of which can thus be analyzed. Higher-order conditioning phenomena allow one to distinguish more precisely between processes involved in transmission of sensory or motor information and processes involved in the plasticity underlying learning. Finally, higher-order conditioning paradigms may also allow one to distinguish between processes involved in behavioral expression of memory retrieval versus processes involved in memory retrieval itself.

Animals↗
PubMed1987

Human learning and memory.

There have been several notable recent trends in the area of learning and memory. Problems with the episodic/semantic distinction have become more apparent, and new efforts have been made (exemplar models, distributed-memory models) to represent general knowledge without assuming a separate semantic system. Less emphasis is being placed on stable, prestored prototypes and more emphasis on a flexible memory system that provides the basis for a multitude of categories or frames of reference, derived on the spot as tasks demand. There is increasing acceptance of the idea that mental models are constructed and stored in memory in addition to, rather than instead of, memorial representations that are more closely tied to perceptions. This gives rise to questions concerning the conditions that permit inferences to be drawn and mental models to be constructed, and to questions concerning the similarities and differences in the nature of the representations in memory of perceived and generated information and in their functions. There has also been a swing from interest in deliberate strategies to interest in automatic, unconscious (even mechanistic!) processes, reflecting an appreciation that certain situations (e.g. recognition, frequency judgements, savings in indirect tasks, aspects of skill acquisition, etc) seem not to depend much on the products of strategic, effortful or reflective processes. There is a lively interest in relations among memory measures and attempts to characterize memory representations and/or processes that could give rise to dissociations among measures. Whether the pattern of results reflects the operation of functional subsystems of memory and, if so, what the "modules" are is far from clear. This issue has been fueled by work with amnesics and has contributed to a revival of interaction between researchers studying learning and memory in humans and those studying learning and memory in animals. Thus, neuroscience rivals computer science as a source of interdisciplinary stimulation. Research on topics such as memory for spatial location, the relation between memory and affect, and autobiographical memory reminds us that general theories of memory based on studies of verbal materials alone are limited. Investigating how people remember complex natural events should provide us with a larger set of memory phenomena to explain and consequently insight into a wider range of memory principles or a deeper understanding of the ones we already accept (e.g. the role of repetition, encoding specificity), including their functional significance for human behavior.(ABSTRACT TRUNCATED AT 400 WORDS)

Affect↗
PubMed1995

Verbal learning and memory in newly diagnosed partial epilepsy.

Verbal learning and memory of 56 adults with newly diagnosed partial epilepsy and no other known brain pathology were compared with memory performance of a normal control group. Memory was evaluated with a list learning test and with recall of logical prose under both immediate and delayed recall conditions. The patients and the controls did not differ in immediate and delayed recall of logical prose. Also learning and immediate recall of the word list was comparable in both groups. After delay the patients recalled fewer words than the control group (P < 0.001), and the percent retention of words was lower in the patients (P < 0.001). The patients with newly diagnosed epilepsy more frequently exhibited mild verbal memory dysfunction as shown in delayed recall of word list. Moderate memory impairment is seen in a group of patients who have deficits in immediate and delayed memory. Follow-up is needed to find out whether patients with memory deficits at the time of diagnosis are those who develop intractable chronic epilepsy.

Adolescent↗
PubMed1995

Verbal learning and memory in children with myelomeningocele.

Examined verbal learning and memory in children with myelomeningocele using the California Verbal Learning Test (CVLT). Participants included 41 children with myelomeningocele, 8 to 15 years of age, 33 of whom had a history of shunted hydrocephalus, and 41 matched, unaffected controls. Children with myelomeningocele and shunted hydrocephalus performed worse than controls on the CVLT. They recalled as many words as controls on the first learning trial, but acquired words more slowly across trials, so that their overall recall was lower. Their learning was characterized by a pronounced recency effect. Their delayed recall of the original list was worse than controls, but not their recognition. Performance of children with myelomeningocele but without shunts was generally not significantly different from that of the other two groups, although they did demonstrate better long-delay free recall than children with shunts. Myelomeningocele is associated with significant retrieval problems when accompanied by shunted hydrocephalus.

Adolescent↗
PubMed1997

Opposite effects of dopamine D2 and D3 receptors on learning and memory in the rat.

Mesolimbocortical dopamine plays a role in learning and memory. The specific receptor subtypes mediating the effects of dopamine, however, are still unknown. Dopamine D2, D3 and D4 receptors are expressed in the hippocampus and dopamine D3 receptors are present in the septal area, suggesting that these receptor subtypes can contribute to the behavioral effects of dopamine D2-like receptor agonists. We now investigated the role of dopamine D2 and D3 receptors in learning and memory by using the transient amnesia induced by scopolamine in the passive avoidance test as experimental model. The data strongly suggest that both dopamine D2 and D3 receptors mediate the effects of dopamine on the integrative function of learning and memory. In particular, we show that the non-selective dopamine agonist apomorphine prevents the scopolamine-induced disruption of consolidation of the previously acquired passive avoidance behavior. This effect is mediated by receptors belonging to the dopamine D2 family since it was antagonized by (-)-sulpiride and mimicked by quinpirole. Nafadotride, a relatively selective antagonist for dopamine D3 receptors, antagonized scopolamine-induced memory disruption and potentiated the facilitatory effect of quinpirole. Taken together, these results suggest that the effects of dopamine on memory consolidation are the result of a balance between dopamine D2 receptor-mediated facilitation and dopamine D3 receptor-mediated inhibition, and that dopamine D2 and D3 receptors play opposite roles in the control of the mechanisms leading to memory consolidation.

Amnesia↗
PubMed2001

Neural basis of novel and well-learned recognition memory in schizophrenia: a positron emission tomography study.

The level of familiarity of a given stimulus plays an important role in memory processing. Indeed, the novelty/familiarity of learned material has been proven to affect the pattern of activations during recognition memory tasks. We used visually presented words to investigate the neural basis of recognition memory for relatively novel and familiar stimuli in schizophrenia. Subjects were 34 healthy volunteers and 19 schizophrenia spectrum patients. Two experimental cognitive conditions were used: 1 week and again 1 day prior to the PET imaging subjects had to thoroughly learn a list of 18 words (well-learned memory). Subjects were also asked to learn another set of 18 words presented 1 min before the PET experiment (novel memory). During the PET session, subjects had to recognize the list of 18 words among 22 new (distractor) words. Subjects also performed a control task (reading words). A nonparametric randomization test and a statistical t-mapping method were used to determine between- and within-group differences. In patients the recognition of novel material produced relatively less flow in several frontal areas, superior temporal gyrus, insular cortex, and parahippocampal areas, and relatively higher activity in parietal areas, visual cortex, and cerebellum, compared to controls. No significant differences in flow were seen when comparing well-learned memory activations between groups. These results suggest that different neural pathways are engaged during novel recognition memory in patients with schizophrenia compared to healthy individuals. During recognition of novel material, patients failed to activate frontal/limbic regions, recruiting a set of posterior perceptual brain regions instead.

Adult↗
PubMed1997

The nucleus accumbens and learning and memory.

Recent research on the nucleus accumbens (NA) indicates that this brain region is involved in learning and memory processes in a way that is separable from its other well-known roles in behavior, such as motivation, reward, and locomotor activity. These findings have suggested that 1) the NA may be involved in declarative, or hippocampal formation-dependent learning and memory, and not in several other non-declarative forms of learning and memory, and 2) the NA may be selectively involved in certain stages of learning and memory. These characteristics suggest that the NA may be part of a larger striatal system which subserves acquisition and consolidation, but is not a site of long-term storage, of different forms of learning and memory.

Animals↗
PubMed1999

Effects of nocistatin on nociceptin-induced impairment of learning and memory in mice.

We investigated the effects of nociceptin/orphanin FQ and nocistatin on learning and memory function as measured in a step-down type passive avoidance task and spontaneous alternation of Y-maze with mice. Nociceptin (0.5-5.0 nmol/mouse, i.c.v.) 30 min before the training session or Y-maze test, dose dependently shortened the step-down latency and impaired spontaneous alternation, while there was no significant effect of nocistatin (0.5-5.0 nmol/mouse). Interestingly, nocistatin (5.0 nmol) significantly improved the nociceptin (5.0 nmol)-induced impairment of learning and memory without changing motor activity or response to electric shocks. These results suggest that nocistatin, a new biologically active peptide now found to also counteract the impairment of learning and memory induced by nociceptin, plays an important role in the regulation of learning and memory process in the central nervous system.

Animals↗
PubMed2003

Prevention of picrotoxin convulsions-induced learning and memory impairment by nitric oxide increasing dose of L-arginine in rats.

Learning and memory processes were tested in adult male rats using a traditional pole-climbing apparatus 30 min after the administration of L-arginine (500 and 1000 mg/kg), the precursor of nitric oxide (NO), and N-nitro-L-arginine methyl ester (L-NAME) (50 and 100 mg/kg), the inhibitor of NO synthesis. The effects of the convulsant (5.0 mg/kg) and a smaller nonconvulsant (2.5 mg/kg) dose of picrotoxin were tested on learning and memory 120 min and 24 h after their administration. The tests were carried out 30 min after L-arginine in animals treated 120 min previously with the convulsant dose of picrotoxin. A dose-dependent enhancement and an inhibition of learning and memory were observed in animals treated with L-arginine and L-NAME, respectively. The convulsant dose of picrotoxin impaired both learning and memory processes. The effect of picrotoxin was reverted following the administration of L-arginine (1000 mg/kg). An interpretation of these results indicates that convulsions induced by picrotoxin produces learning and memory impairment, and that this defect is reversible if NO synthesis is increased in the brain by the systemic administration of L-arginine.

Animals↗
PubMed2000

Learning and memory impairment in cocaine-dependent and comorbid schizophrenic patients.

Impairments in verbal learning and memory functioning have been found to be cardinal features among individuals with schizophrenia as well as among non-schizophrenic cocaine abusers. Cognitive deficits in these areas, moreover, have been associated with poor treatment response and short-term outcome. Little is known, however, about the acute effects of cocaine abuse on schizophrenic patients' learning and memory functioning. Consequently, a potentially reversible and treatable source of cognitive impairment has been virtually ignored. The present study examined the extent of verbal learning and memory impairment in a group of cocaine-dependent schizophrenic patients (n=42) and a group of non-schizophrenic cocaine-dependent patients (n=21) within 72 h of the last cocaine use using the California Verbal Learning Test (CVLT). Schizophrenic patients (n=34) without any substance-use disorders were also tested in an identical time frame and served as a comparison group. Results revealed that all groups demonstrated significant learning and memory impairment relative to CVLT published age and gender corrected norms. Both cocaine-dependent and non-substance abusing schizophrenic groups presented a very similar pattern of impaired learning and recall performance across all CVLT task domains. Comorbid patients, in contrast, presented with marked deficits in their ability to learn and recall verbal information relative to either schizophrenic or cocaine-only groups. Moreover, the cocaine-abusing schizophrenic patients showed significant forgetfulness of the information that they did acquire during delayed recall conditions. The performance deficits exhibited by cocaine-abusing schizophrenic patients differed not only in relative severity of impairment, but also qualitatively in their increased rates of forgetfulness of acquired information. These results are interpreted in terms of the neurobiological substrates of learning and memory and the neurobiological impact of cocaine on schizophrenic patients' cognition during the early phase of inpatient hospitalization. These results suggest that comorbid patients should be targeted for specialized remediation efforts at the beginning phases of inpatient treatment.

Acute Disease↗
PubMedDate not supplied

Tyrosine administration prevents hypoxia-induced decrements in learning and memory.

Exposure to hypobaric hypoxia rapidly produces decrements in learning and memory. Tyrosine, a neurotransmitter precursor, has beneficial behavioral effects when administered to animals and humans exposed to various acute stressors. To determine whether tyrosine would protect rats from the adverse effects of hypobaric hypoxia on spatial reference and working memory, it was administered to 27 male Fischer 344 rats tested in the Morris water maze. Rats were tested starting at 2 and 6 h of an 8 h exposure to a simulated altitude of 5950 m (19,500 ft) or sea level. Tyrosine or placebo was administered 1/2 h prior to each testing session (400 mg/kg, IP). Altitude exposure significantly increased working memory escape latency; treatment with tyrosine reversed this decrement. There was no effect of altitude or tyrosine on reference memory. There were also no treatment-related differences in performance when animals were tested the next day at sea level. The beneficial effects of tyrosine on working memory performance may be due to a direct effect of tyrosine on memory, alleviation of a hypoxia-induced retardation of learning, or to other central or peripheral effects of this dietary catecholamine precursor.

Altitude↗
PubMed1997

[Memory and learning: 'experience' and 'skill' of the brain].

OBJECTIVE: To describe the current typology and different processes involved in memory and learning, as well as adequate tests in the diagnosis of the mnesic disorders. DEVELOPMENT: We reviewed the most recent studies about functional and lesional neuroanatomy of memory and learning and their neurophysiological bases (cellular and biochemical), with special emphasis in studies published in the three last years. We structured a typological classification, we expose the processes involved in short-term and long-term memory, we detailed the mnesic processes of declarative and implicit type, and we expose profiles of amnesias frequent in the clinical neurology and neuropsychology. CONCLUSIONS: Memory is not a diffuse and unitary process in our brain, neither amnesia is an absolute loss of memory. The multidimensional combination of two temporary memories (short- and long-term) and three mnesic processes ('working memory', explicit and implicit memory-learning) increases our capacity to memorize and learn, and it allows us to store the information in distinctive periods, with different mechanisms and covering different necessities. Patients with amnesia exhibit distinctive profiles of mnesic processes affected.

Brain↗