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PubMed2005

Latent factor structure of the Test of Memory and Learning in a pediatric traumatic brain injured sample: support for a general memory construct.

The Test of Memory and Learning (TOMAL; Reynolds, C. R., & Bigler, E. D. (1994a). Test of Memory and Learning (TOMAL). Austin, Texas: Pro-Ed; Reynolds, C. R., & Bigler, E. D. (1994b). Test of Memory and Learning (TOMAL): Examiner's manual. Austin, Texas: Pro-Ed) was published to ameliorate the paucity of developmentally appropriate instruments for the assessment of memory in children and adolescents. No studies have confirmed the latent factor structure of the TOMAL. Two structural models were subjected to confirmatory factor analysis using the TOMAL performances of 140 subjects, age 5-19, with traumatic brain injury (TBI). Model 1 was a four-factor model with a large "Complex Memory" factor and three smaller factors. Model 2 was a two-factor model with Verbal and Nonverbal Memory factors, both of which loaded on a second-order "General" memory factor. Results indicated that the model with a higher order structure demonstrated better fit than the four-factor model. Further analysis suggested that the TOMAL factor structure is characterized by a large Complex Memory and smaller, Sustained Attention factor. The study provides tentative support for a "general memory" construct.

Adolescent↗
PubMedDate not supplied

Behavioral methods for measuring effects of drugs on learning and memory in animals.

This review describes methods for measuring effects of drugs on learning and memory in animals, proceeding from relatively simple nonassociative learning (habituation) to classical and instrumental conditioning, and concluding with complex measures for measuring learning and memory repeatedly in the individual animal. Procedures for separating drug effects specific to learning and memory from non-specific effects on activity, motivation, sensory and motor capacity, etc., were emphasized. For each method, selected experimental examples were presented which described the action of drugs on learning and memory, elucidated the behavioral processes involved in the drug effects, or illustrated methodological points. The various procedures used to measure drug effects on learning and memory in animals have yielded a bewildering array of often-contradictory results. Quantitative differences in effectiveness of drugs in the different procedures are common. Drugs (for example, the nootropics) that alter learning or memory in a few procedures may be totally without activity in many others. How are these discrepancies to be interpreted? The apparent inconsistencies in the data can, for the most part, be understood in terms of the nature of learning and memory. "Learning" and "memory" are hypothetical processes presumed to underlie enduring changes in behavior resulting from the organism's interaction with environmental stimuli. Given such a broad definition, the prevalence of inconsistencies in the data is hardly surprising. It is unlikely that the same mechanisms should underlie all of the wide variety of behavioral changes included under the rubrics "learning" or "memory." (For a contrary view, based on consistencies among results obtained in the diverse procedures, see Zornetzer). How, then, should drug effects on learning and memory be identified or measured? The first step, of course, is to rule out those drug effects that do not conform to the definition of learning or memory. This review has described strategies and procedures by which this can be accomplished. However, even when this is done there is no single procedure that can detect drug effects on learning and memory in general, nor, in view of the heterogeneous behaviors involved, is it likely that such a universal procedure will ever be found. Thus, a multi-faceted strategy will be required. Some of the simpler procedures described in this review may be adequate for the initial identification of interesting effects.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1999

Genetic enhancement of learning and memory in mice.

Hebb's rule (1949) states that learning and memory are based on modifications of synaptic strength among neurons that are simultaneously active. This implies that enhanced synaptic coincidence detection would lead to better learning and memory. If the NMDA (N-methyl-D-aspartate) receptor, a synaptic coincidence detector, acts as a graded switch for memory formation, enhanced signal detection by NMDA receptors should enhance learning and memory. Here we show that overexpression of NMDA receptor 2B (NR2B) in the forebrains of transgenic mice leads to enhanced activation of NMDA receptors, facilitating synaptic potentiation in response to stimulation at 10-100 Hz. These mice exhibit superior ability in learning and memory in various behavioural tasks, showing that NR2B is critical in gating the age-dependent threshold for plasticity and memory formation. NMDA-receptor-dependent modifications of synaptic efficacy, therefore, represent a unifying mechanism for associative learning and memory. Our results suggest that genetic enhancement of mental and cognitive attributes such as intelligence and memory in mammals is feasible.

Animals↗
PubMed1989

Region selective increase in activities of CNS cholinergic marker enzymes during learning of memory tasks in aged rats.

The effects of learning memory tasks on activities of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) in the frontal cortex (FC), hippocampus (HC) and cerebellum of aged rat brains were studied in comparison with those of young adult rats. Aged rats were significantly inferior than young adult rats in both active avoidance (two-way shuttle box) and water-filled multiple T-maze learning. ChAT activity in the FC of aged rats was significantly increased after 5 days of training in an active-avoidance learning task. ChAT activity in the HC of aged rats was also significantly increased after 6 days of training in a water-filled multiple T-maze. These changes did not occur in young adult rats after either 2 or 5 days of active avoidance training, or in aged rats after 10 days of training, both of which were after the maximum level of learning of active avoidance task had been attained. AChE activity was significantly lower in the FC and HC of nontrained aged rats when compared with that of nontrained young adult rats. The reduced activity of AChE in both brain regions of nontrained aged rats rose to almost the same level as that in young adult rats in nontrained and trained states in an active avoidance task. From these findings, it is hypothesized that the task-dependent elevation in the activities of the central nervous system (CNS) cholinergic marker enzymes in trained aged rats may be compensatory changes to keep a relevant level of neurotransmission in the face of specific motor and/or cognitive insults.

Acetylcholinesterase↗
PubMed2002

Age-related biophysical alterations of hippocampal pyramidal neurons: implications for learning and memory.

Normal brain aging is associated with deficits in learning and memory. The hippocampus, a structure critical for proper learning and memory functions, is frequently implicated in aging-related learning deficits. There are many reports of learning-related changes in hippocampal pyramidal neurons from animals that were trained in hippocampus-dependent learning paradigms. One consistent finding in hippocampal pyramidal neurons is a learning-related increase in postsynaptic neuronal excitability, resulting from a reduction in the postburst afterhyperpolarization (AHP). The hippocampus, as well as the ability to acquire hippocampus-dependent tasks, is particularly affected by aging. Correspondingly, hippocampal neurons also display an age-related decrease in excitability, resulting from an enhanced AHP. The correlation between neuronal excitability and learning ability strongly suggests that changes in the AHP are critically involved in learning and age-related learning deficits. Additional support for this argument comes from in vitro studies that examined the effect of compounds that facilitated learning in aging animals on the properties of CA1 pyramidal neurons. Many of these compounds increased the excitability of CA1 pyramidal neurons by reducing the AHP. Subsequent voltage-clamp recordings showed that AHP reduction by these compounds mainly reflects the reduction of two of its currents, the I(AHP) and the sI(AHP). Conversely, age-related AHP enhancements primarily impact the I(AHP) and the sI(AHP). Given that the I(AHP) accounts for a small portion of the total AHP, and that the sI(AHP) is the AHP current that most critically modulates neuronal excitability, changes in neuronal excitability seen in learning and in aging are predominantly caused by changes in the sI(AHP). The fact that the sI(AHP) receives neuromodulation from many transmitter systems important for learning and sensitive to aging lends further support for its role in age-related learning deficits. In this article, we review: (1) two hippocampus-dependent learning tasks, trace eyeblink conditioning and Morris water maze training, that are used extensively in our laboratory to examine learning and aging-related learning deficits; (2) aging-related changes in several important neurotransmitter systems, and how the these changes impact learning and memory functions during aging; and (3) changes in the AHP and the sI(AHP) in hippocampal pyramidal neurons in relation to compromised neurotransmission, as well as to learning, in aging animals. The correlations between a reduction in the sI(AHP) in learning, and an enhancement in the sI(AHP) in aging provide compelling evidence that this current plays a critical role in cognitive functions, and further suggest that the key modulators of the AHP are good candidates for future therapeutic interventions in age-related neurodegenerative diseases.

Aging↗
PubMed2006

Alterations in spatial learning and memory after forced exercise.

Exercise has been shown to influence learning and memory. Most studies were performed with a voluntary running paradigm (e.g. running wheel) in mice. However, such effects of exercise on learning and memory are less well demonstrated using a forced running paradigm (e.g. treadmill). The present study was designed to examine the effects of 12 weeks of forced treadmill running on learning and memory performance in rats. We have previously shown that forced running resulted in qualitative and quantitative changes in the cholinergic neurons of the horizontal diagonal band of Broca (HDB) in the septum. This study was conducted in order to determine whether or not these changes occur simultaneously with enhanced learning and memory. The one-day version of the Morris water maze (MWM) test [Frick, K.M., Stillner, E.T., Berger-Sweeney, J., 2000. Mice are not little rats: species differences in a one-day water maze task. NeuroReport 11, 3461-3465] was used to test spatial learning and memory after the exercise period. Our data showed that runners displayed better spatial learning and memory when compared to nonrunners. This was evidently shown by a reduction in the time required for spatial acquisition (p<0.05) and superior probe trial performance (p<0.05). A shorter distance swam by the runners also suggested improved learning over the nonrunners (p<0.05). In an attempt to revalidate our earlier quantitative results, we used design-based stereology (DBS) to estimate the number of cholinergic neuronal profile population in the medial septum and diagonal band (MSDB). We confirmed that forced running increased the cholinergic neuronal profile subpopulation in the HDB (Coefficient of Error<0.2). Taken together, these results indicate that forced exercise could influence learning and memory with a concomitant increase in the number of cholinergic neurons in the HDB.

Acetylcholinesterase↗
PubMed1997

Drosophila learning and memory: recent progress and new approaches.

The processes of learning and memory have traditionally been studied in large experimental organisms (Aplysia, mice, rats and humans), where well-characterized behaviors are easily tested. Although Drosophila is one of the most experimentally tractable organisms, it has only recently joined the others as a model organism for learning and memory. Drosophila behavior has been studied for over 20 years; however, most of the work in the learning and memory field has focused on initial learning, because establishing memory in Drosophila has not been as straightforward as in other organisms. A major recent advance in this field has been the development of a training protocol that induces long-term memory in files. This made possible experiments that implicated the Drosophila CREB gene as a critical component in the consolidation of long-term memory, and paves the way for future experiments utilizing the well developed tools in Drosophila. This review will briefly summarize what is known in the field of Drosophila learning and memory to date, and discuss why the unique aspects of this field make traditional approaches difficult and reward the use of alternative paths of experimentation.

Animals↗
PubMed2004

Verbal learning and memory after childhood stroke.

Verbal learning and memory (VLM) following pediatric stroke was characterized in a cross-sectional neuropsychological and neuroimaging study of 26 subjects, aged 5 to 17, with a history of pediatric stroke and 26 age, SES, and gender matched orthopedic controls. Further comparisons were made between the VLM profiles of stroke subjects with right versus left hemisphere lesions and early (> 12 months) versus late (12 months) strokes. Overall, stroke subjects scored significantly lower than control subjects on several VLM indices (California Verbal Learning Test-Children; CVLT-C), as well as on measures of intellectual functioning (IQ) and auditory attention/working memory (Digit Span). Subgroup analyses of the stroke population found no significant differences in VLM, Digit Span, Verbal IQ or Performance IQ when left-hemisphere lesion subjects were compared to right-hemisphere lesion subjects. In contrast, early strokes were associated with significantly fewer words recalled after delay, reduced discriminability (fewer correct hits relative to false positive errors on recognition testing), and relatively worse auditory attention/working memory scores (Digit Span). These findings indicate that pediatric stroke subjects demonstrated more VLM impairment than control subjects, and early strokes were associated with greater recall and recognition deficits. In stark contrast with adult-onset stroke, both left- and right-hemisphere lesions during childhood resulted in similar VLM performance.

Adolescent↗
PubMed1993

Differential effects of dunce mutations on associative learning and memory in Drosophila.

Initial learning, 30- and 180-min memory retention after Pavlovian conditioning of an odor avoidance response was quantified in dnc1, dnc2, dncM11 and Canton-S (wild-type) homozygotes and in dnc1/FM7, dnc2/FM7, dncM11/FM7, dncM11/Can-S, Can-S/FM7, dnc1/dncM11 and dnc2/dncM11 heterozygotes. Our results consistently showed that a) the dunce mutations are semi-dominant for initial learning and b) genetic variants carrying the enzymatically hypomorphic dnc2 mutation produce learning scores lower than those of the amorphic dncM11. Analysis of this particular set of retention intervals, using a modified statistical model designed to evaluate decay rates, revealed no discernable effects of the dunce mutations on memory formation 30 to 180 min after training. These results are consistent with a model of memory formation, in which dunce is hypothesized to disrupt acquisition and/or short-term memory.

Animals↗
PubMed2006

A critical role for the glial-derived neuromodulator D-serine in the age-related deficits of cellular mechanisms of learning and memory.

Age-associated deficits in learning and memory are closely correlated with impairments of synaptic plasticity. Analysis of N-methyl-D-aspartate receptor (NMDAr)-dependent long-term potentiation (LTP) in CA1 hippocampal slices indicates that the glial-derived neuromodulator D-serine is required for the induction of synaptic plasticity. During aging, the content of D-serine and the expression of its synthesizing enzyme serine racemase are significantly decreased in the hippocampus. Impaired LTP and NMDAr-mediated synaptic potentials in old rats are rescued by exogenous D-serine. These results highlight the critical role of glial cells and presumably astrocytes, through the availability of D-serine, in the deficits of synaptic mechanisms of learning and memory that occur in the course of aging.

Aging↗
PubMed1988

Clinical relevance of effects of benzodiazepines on learning and memory.

The effects of benzodiazepines on learning and memory are examined in the various clinical situations in which these drugs are used. Alterations in performance arising from the conditions for which benzodiazepines are prescribed are also considered. Current evidence indicates that, in anxious patients, as in normal volunteers, benzodiazepines impair the acquisition of new information (episodic memory). Although some tolerance may develop to these impairments, deficits are observed even after patients have been taking their medication chronically. Like amnesic patients, benzodiazepine-treated subjects may be unaware of their impaired ability to learn. The effects of the impairments on behavioral psychotherapies are considered.

Anti-Anxiety Agents↗
PubMed1997

Isolated-brain parallels to simple types of learning and memory in Tritonia.

Physiological studies of learning and memory often require reduced nervous system preparations that can be trained by stimulation of neural pathways in a manner that mimics behavioral training. In the isolated brain preparation of the seaslug Tritonia, fictive swimming can be activated with a few electrical pulses applied to the cut end of a nerve, and learning experiments can be simulated with combinations of nerve stimuli. Repeated application of a nerve stimulus produced changes in fictive swimming that resembled habituation and iterative enhancement of multiple components of the swimming behavior. Many repetitions of the nerve stimulus led to fictive swimming failure. Stimulation of another nerve then restored the ability of the original nerve to activate fictive swimming, thus reproducing dishabituation results. Sensitization of threshold and latency were also simulated. Parallels between the behavior and the isolated brain suggest that the neuronal modifications underlying simple types of learning can be induced by nerve stimulation. The activity pattern of interneuron C2 in these experiments suggests that increased C2 synaptic efficacy may underlie sensitization of swimming latency.

Action Potentials↗
PubMed2005

Effect of naloxone on aluminum-induced learning and memory impairment in rats.

BACKGROUND: Uptake of aluminum may disturb the learning and memory of humans or animals. Naloxone (NAL) has been shown to exert beneficial effects on memory deficits. AIMS: We investigated the effects of naloxone on aluminum-induced learning and memory impairment in rats. SETTINGS AND DESIGN: Aluminum-induced learning and memory impairment model was established by gavage of Aluminum chloride (600 mg/kg) for 3 months. Rats were divided into three groups viz. naloxone-treated rats (NAL 0.8 mg/kg, i.p. daily for 7 days), non-treated model rats and normal controls. MATERIALS AND METHODS: The Morris water maze test was performed to study spatial learning and memory. Long-term potentiation (LTP) of the Schaffer collateral-CA1 synapse was recorded. Aluminum and zinc contents in the hippocampus were assayed with atomic absorption spectrophotometry. STATISTICAL ANALYSIS: Parameters of the hidden and visible platform trials and data of LTP were analyzed using two-way repeated measures ANOVA. RESULTS: In the hidden platform trials, escape latencies of the NAL rats were significantly shorter than that of the non-treated rats (P=0.000, 95% confidential interval low bound 14.31, upper bound 22.68). In probe trails, the number of entries in the target area of the NAL rats (6.75+/-1.28 times/min) was more than that of non-treated model rats (4.56+/-2.16 times/min, P=0.004, 95% confidence interval low bound -3.65, upper bound -0.788). The magnitudes of LTP recorded in the CA1 pyramidal neurons of the NAL-treated rats were significantly augmented when compared to the non-treated model rats (P=0.005, 95% confidence interval low bound 0.16, upper bound 0.84). CONCLUSIONS: NAL could facilitate spatial learning and memory and enhance LTP in the CA1 region of the hippocampus in aluminum-induced learning and memory impairment in rats.

Aluminum↗
PubMed2001

The neurobiology of learning and memory: some reminders to remember.

We have learned much about the neurobiology of learning and memory in the past 100 years. We have also learned much about how we should, and should not, investigate these complex processes. However, with the rapid recent growth in the field and the influx of investigators not familiar with this past, these crucial lessons too often fail to guide the research of today. Here we highlight some major lessons gleaned from this wealth of experience. These include the need to carefully attend to the learning/performance distinction, to rely equally on synthetic as well as reductionistic thinking, and to avoid the seduction of simplicity. Examples in which the lessons of history are, and are not, educating current research are also given.

Animals↗
PubMedDate not supplied

Sensory responsiveness and the effects of equal subjective rewards on tactile learning and memory of honeybees.

In tactile learning, sucrose is the unconditioned stimulus and reward, which is usually applied to the antenna to elicit proboscis extension and which the bee can drink when it is subsequently applied to the extended proboscis. The conditioned stimulus is a tactile object that the bee can scan with its antennae. In this paper we describe the quantitative relationships between gustatory antennal stimulation, gustatory proboscis stimulation, and tactile learning and memory. Bees are 10-fold more responsive to sucrose solutions when they are applied to the antenna compared to proboscis stimulation. During tactile conditioning, the sucrose solution applied to the proboscis determines the level of acquisition, whereas antennal input is of minor importance. Bees differing in their gustatory responsiveness measured at the antenna differ strongly in their tactile acquisition and memory. We demonstrate how these differences in tactile acquisition and memory can be greatly reduced by calculating equal subjective rewards, based on individual gustatory responsiveness.

Animals↗
PubMed1998

Operant visual learning and memory in Drosophila mutants dunce, amnesiac and radish.

Learning and memory of Drosophila mutants dunce, amnesiac and radish which were isolated originally from the classical olfactory learning paradigm are analyzed in an operant visual learning paradigm. Dunce appears to show normal ability to learn during training, but its memory is significantly affected. Though the learning index during the first minute after training is normal, its short-term memory (STM), anesthesia-resistant memory (ARM) and long-term memory (LTM) are all significantly damaged. Amnesiac displays disrupted middle-term memory (MTM), while its STM and LTM remain unchanged. Learning and memory in radish mutants seem to be unaffected. These results lend support to the argument that there are certain common molecular mechanisms underlying learning and memory through different tasks and the previous multi-phase model of visual memory is modified in a genetic way.

Journal Article↗
PubMed1998

Effects of U-50,488H on scopolamine-, mecamylamine- and dizocilpine-induced learning and memory impairment in rats.

The role of kappa opioid receptor agonists in learning and memory is controversial. In the present study, the effects of U-50,488H on scopolamine-, mecamylamine- and dizocilpine-induced learning and memory impairments in rats were investigated. Scopolamine (3.3 mumol/kg s.c.), a muscarinic cholinergic antagonist, and mecamylamine (40 mumol/kg s.c.), a nicotinic cholinergic antagonist, significantly impaired learning and memory in rats in a step-through type passive avoidance test. Administration of U-50,488H (0.17 or 0.51 mumol/kg s.c.) 25 min before the acquisition trial reversed the impairment of learning and memory induced by scopolamine and mecamylamine. Although low doses of scopolamine (0.17 mumol/kg) and mecamylamine (12 mumol/kg) had no effect, concurrent administration of both antagonists induced impairment of learning and memory. Scopolamine significantly increased acetylcholine release in the hippocampus as determined by in vivo brain microdialysis. On the other hand, mecamylamine significantly decreased acetylcholine release. U-50,488H completely blocked the decrease in acetylcholine release induced by mecamylamine, whereas it only partially blocked the increase of acetylcholine induced by scopolamine. On the other hand, an endogenous kappa opioid receptor agonist, dynorphin A (1-13), did not block the increase in acetylcholine release induced by scopolamine. The antagonistic effect of U-50,488H was abolished by pretreatment with nor-binaltorphimine (4.9 nmol/rat i.c.v.), a selective kappa opioid receptor antagonist. 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 U-50,488H reverses the impairment of learning and memory induced by the blockade of cholinergic transmission and abolishes the decrease of acetylcholine release induced by mecamylamine via the kappa receptor-mediated opioid neuronal system.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed2002

Lateralization of spatial-memory processes: evidence on spatial span, maze learning, and memory for object locations.

Spatial memory is one of the most important cognitive functions in daily life, enabling us to locate objects in our environment or to learn a route or a path. In the present study, we elaborated on the hypothesis that human spatial memory consists of multiple sub-processes, relying on different brain structures. Therefore, 50 patients with an ischemic stroke and 40 healthy participants underwent tests measuring spatial span and maze learning. By means of a computer paradigm the following aspects of memory for object locations were assessed: (1) object location binding; (2) positional memory; (3) a combination of these two aspects. The results clearly showed a double dissociation: the group of patients with an infarct in the left hemisphere (LH) was impaired on object location binding, whereas the group with an infarct in the right hemisphere (RH) was impaired on positional memory. Lesions in the RH resulted also in impairments on maze learning. Moreover, patients with lesions in the posterior part of the parietal or the occipital lobe performed especially worse on spatial-memory tasks. These findings extend the theoretical framework of categorical versus coordinate spatial processing in the human brain and corroborate previous findings on selective aspects of memory for object locations.

Adult↗