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E-service learning: A pedagogic innovation for healthcare management education.

This paper proposes an innovation in service learning that we identify as e-service learning. By adding the "e" to service learning, we create a service learning model that is dynamic, mediated by technology, and delivered online. This paper begins by examining service learning, which is a distinct learning concept. Service learning furnishes students with opportunities for applied learning through participation in projects and activities in community organizations. The authors then define and conceptualize e-service learning, including the anticipated outcomes of implementation such as enhanced access, quality, and cost effectiveness of healthcare management education. Because e-service learning is mediated by technology, we identify state of the art technologies that support e-service learning activities. In addition, possible e-service learning projects and activities that may be included in healthcare management courses such as finance, human resources, quality, service management/marketing and strategy are identified. Finally, opportunities for future research are suggested.

Curriculum↗

Effects of a metacognitive intervention on students' approaches to learning and self-efficacy in a first year medical course.

AIM: To determine the influence of metacognitive activities within the PBL tutorial environment on the development of deep learning approach, reduction in surface approach, and enhancement of individual learning self-efficacy. METHOD: Participants were first-year medical students (N = 213). A pre-test, post-test design was implemented with intervention and control cohorts, with intervention students experiencing a program of metacognitive activities within their PBL tutorials of at least 20 weeks duration. All students completed the Medical Course Learning Questionnaire at the commencement, and again at the completion of, the study. The metacognitive intervention itself consisted of reflection on the learning in PBL coupled with peer- and self-assessment. RESULTS: Self-efficacy was significantly reduced for both control and intervention cohorts at the conclusion of the study. A significant reduction in the adoption of deep and strategic learning approach, matched by a corresponding increase in the use of surface learning, was demonstrated for both cohorts. There was a statistically significant association between high self-efficacy and deep learning approach, with older students over-represented in the group of efficacious deep learners. CONCLUSION: Over the course of first-year medical studies, students lose self-efficacy and move away from deep-strategic learning approaches towards more surface approaches. The program of metacognitive activities failed to reverse this trend. The substantial swing towards surface learning raises questions about the perceived capacity of PBL curricula to promote deep approaches to learning in dense curricula, and reinforces the importance of personal and contextual factors, such as study habits, workload and assessment, in determining individual approaches and idiosyncratic responses to learning situations.

Adult↗

Disorders of learning and memory processes in a monkey model of Alzheimer's disease: the role of the associative area of the cerebral cortex.

The processes of learning and storage of the results of learning were studied in a model of Alzheimer's disease in two groups of rhesus macaques (three individuals in each group). Studies were performed after injection of neurotoxins (group I) and physiological saline (group II, controls). Two months after injections (stage C1), learning parameters were studied in monkeys of both groups using a new stimulus discrimination test (filled geometrical figures versus outline figures). There were significant differences between the animals of the two groups. Learning was hindered in monkeys of group I, with significant increases in the learning time (the time to achieve a stable probability of correct responding of 0.85) and in the probability of refusals. Monkeys of group II showed no learning impairment. Animals were trained to discriminate new stimuli (images of two monkeys) six months after injections (stage C3). Learning was impaired in animals of group I, such that learning measures had the same levels as previously; monkeys of group II showed no learning impairment. Analysis of the characteristics of working memory, which is involved in storing the results of new learning, was performed at stage C1; monkeys of group I showed significant degradation of these measures, with a significant decrease in the probability of correct solutions at stage C1 (to a level of 0.5), with some increase at stages C2 (at four months) and C3, along with a significant increase in the probability of refusals, values being similar at all time points. For monkeys of group II, these characteristics showed no degradation. Motor response times at stages C1, C2, and C3 were not different for the two groups of monkeys. The structural-functional organization of interactions between sensory and cognitive processes during learning and the storage of information in working memory are discussed, as is the role of the associative areas of the cortex in these interactions.

Alzheimer Disease↗

Effects of social isolation rearing on learning in the Morris water maze.

Impaired learning has been shown as a consequence of isolation-rearing in a variety of paradigms. However, there are situations in which learning in isolation-reared rats is enhanced or unimpaired compared to socially reared rats. The present experiments investigated the effects of isolation rearing on place navigation in the Morris water maze. Two complementary paradigms were studied: isolation and socially reared rats were exposed to the water maze either without drug pretreatment or following systemic administration of scopolamine. Two conditions were examined: place learning and reversal learning. Male Lister hooded rats were either housed singly (isolation reared) or in groups of four (social reared) from weaning at 21 days of age. Six weeks later place learning and reversal learning were determined using the Morris water maze. The time taken to locate the submerged island (escape latency) was used as the measure of learning ability. The results showed that place learning, and reversal learning were enhanced in isolation reared rats compared to socially reared controls. Pretreatment with scopolamine (0.3 and 0.5 mg/kg, i.p.) produced a dose-related cognitive deficit as shown by an increase in the escape latency. Scopolamine (0.3 mg/kg) impaired both place and reversal learning but this was less pronounced in isolation compared to socially-reared rats. These results suggest that rearing in isolation may enhance spatial learning though central cholinergic mechanisms.

Animals↗

Learning-memory deficit with aging in APP transgenic mice of Alzheimer's disease and intervention by using tetrahydroxystilbene glucoside.

OBJECTIVE: To investigate learning-memory deficit in different ages of AD-like APP transgenic mice and to observe the protective effects of 2,3,5,4'-tetrahydroxystilbene-2-O-beta-D-glucoside (TSG), which is the main component of Polygonum multiflorum, on learning-memory abilities. METHODS: PDAPPV717I transgenic (Tg) mice were randomly divided into 3 model groups (4, 10 and 16 months old mice) and TSG treated (at doses 120 and 240 micromol/kg/d) groups. TSG was administered to some Tg mice with an age range 4-10 months. In untreated 10 months old Tg mice, the TSG was administrated to those falling in the age range 10-16 months. For the control group we adopted the same age and background C57BL/6J mice. The learning-memory ability was measured by applying Morris water maze (MWM) and object recognition test (ORT). RESULTS: In the 4 months old PDAPPV717I Tg mice, the learning-memory deficit was detected. The escape latency in MWM was prolonged, and the discrimination index decreased in ORT. In the 10 months old Tg mice, the learning-memory deficit was aggravated. TSG improved all spatial learning-memory impairment in MWM as well as the object recognition impairment in ORT. In the 16 months old Tg mice, the learning-memory deficit remained to exist but abated a lot. TSG showed significant improvement in learning-memory ability in both MWM and ORT. CONCLUSION: PDAPPV717I transgenic mice with an age range 4-16 months revealed the existence of learning-memory deficit compared with the control group. Tetrahydroxystilbene glucoside not only prevents, i.e. at an early stage, the learning-memory deficit in AD-like model, but also can reverse the learning-memory deficit in the late stage of AD-like model. Thus, TSG could be considered among the future therapeutic drugs indicated for the treatment of AD.

Age Factors↗

Severe learning impairment caused by combined immunotoxic lesion of the cholinergic projections to the cortex and hippocampus in monkeys.

Monkeys with immunotoxic lesions of both the basal nucleus of Meynert and the vertical limb of the diagonal band of Broca (NBM+VDB) lost cholinergic innervation throughout the cortex and hippocampus. They were impaired at learning discriminations between objects differing in either few, or many, attributes and at learning visuospatial conditional discriminations. Monkeys with immunotoxic lesions of the NBM lost cholinergic innervation of the neocortex only. Initially, they were unable to learn a simple visual discrimination where the stimuli differed in a limited number of attributes but they were unimpaired at learning discriminations between objects that differed in more attributes. They were mildly impaired at learning a visuospatial conditional task. The impairment exhibited by monkeys with lesions of the NBM alone ameliorated with time but that following NBM+VDB lesions did not. Previous experiments have shown that monkeys with immunotoxic lesions of the VDB alone are impaired at learning visuospatial conditional discriminations but are unimpaired at learning simple visual discriminations. When monkeys with NBM lesions were given excitotoxic lesions of the CA1 field of the hippocampus the learning impairment on discriminations between objects which differed in few attributes was reinstated. Pretreatment with a cholinergic agonist improved learning ability on visual discrimination learning in all monkeys but this improvement was significantly greater in monkeys with lesions of the NBM. On conditional discrimination learning, which is particularly sensitive to hippocampal damage, pilocarpine produced a significant improvement in monkeys with NBM+VDB lesions (where the hippocampal dysfunction was cholinergic) but not in monkeys with NBM+CA1 lesions (where the hippocampal damage was structural).

Acetylcholine↗

Learning-induced alterations in hippocampal PKC-immunoreactivity: a review and hypothesis of its functional significance.

1. To localize protein kinase C (PKC) in the hippocampus, PKC activity measures, mRNA in situ hybridization, and [3H]phorbol ester binding techniques were used until in the 1980s antibodies became available for in situ immunocytochemistry. In the late 1980s, PKC-isoform-specific antibodies were first used to map hippocampal PKC at the cellular and subcellular level. The mammalian hippocampus contains all four Ca(2+)-dependent PKC isoforms, but the (sub)cellular localization is both isoform- and species-specific. 2. Hippocampally-dependent spatial and associative learning in rat, mice and rabbit induce an increase in PKC immunoreactivity (ir) in hippocampal principal cells studied 24 hours after the animals had learned the task. Among the four Ca(2+)-dependent PKC subtypes, this increase is selective for the gamma-isoform. The presence of the gamma-isoform in dendritic spines (the most likely site for synaptic plasticity and information storage), in contrast to PKC alpha, beta 1, and beta 2, may underlie the isoform-selectivity. 3. Compared to fully trained animals, subjects halfway training showed intermediate levels of increased PKC gamma-ir. Poor learners that were not able to learn the task showed considerably less enhanced PKC gamma-ir as compared to good learners. 4. Associative learning induced a decrease in astroglial PKC beta 2 and gamma-ir in those regions where a simultaneous increase in neuronal PKC gamma-ir was observed. This decrease most likely reflects PKC down-regulation, enabling the astrocytes to maintain their K+ buffering capacity necessary to support neuronal activity such as accompanying learning and memory. 5. Western blot analyses revealed that the increase in PKC gamma-ir was not due to an increase in total amount of PKC gamma, translocation, or the proteolytic generation of the fragment PKM. The increase in PKC gamma-ir must therefore reflect a learning-induced conformational change in the PKC gamma molecule that results in the exposure of the antigenic site(s). 6. Although a large number of hippocampal pyramidal cells display learning-induced enhancement of PKC gamma-ir at the 24 hours post-training time point, this does not indicate, however, that all synapses in these neurons are used, or that the maximal PKC signal transduction capacity per call has been reached. 7. The enhanced PKC gamma-ir may reflect a form of activated PKC, since PKC stimulation by phorbol esters (both in hippocampal slices and mildly aldehyde fixed sections) mimicked the increase in PKC gamma-ir similar as seen after learning. 8. The most likely transmitter systems which may have induced the altered PKC gamma-ir are acetylcholine and glutamate. Their contribution and interaction at the cellular level are depicted in a schematic circuit terminating on a CA1 pyramidal cell (Fig. 4). 9. Several functional roles for PKC gamma in learning and memory are discussed, and a hypothetical model is proposed based on an endogeneous PKC inhibitor protein that may explain altered antibody-binding to PKC gamma after learning (Fig. 6). 10. The immunocytochemical approach can contribute significantly to the ongoing attempts to decipher part of the cellular and biochemical mechanism of learning and memory. The development of ever more specific and better characterized antibodies reactive with different sites of proteins like PKC gamma will offer the necessary tools for further immunocytochemical research to help unravel complex brain functions.

Animals↗

Place versus response learning revisited: tests of blocking on the radial maze.

Neurobiological and behavioral research indicates that place learning and response learning occur simultaneously, in parallel. Such findings seem to conflict with theories of associative learning in which different cues compete for learning. The authors conducted place+response training on a radial maze and then tested place learning and response learning separately by reconfiguring the maze in various ways. Consistent with the effects of manipulating place and response systems in the brain (M. G. Packard & J. L. McGaugh, 1996), well-trained rats showed strong place learning and strong response learning. Three experiments using associative blocking paradigms indicated that prior response learning interferes with place learning. Blocking and related tests can be used to better understand how memory systems interact during learning.

Animals↗

The effectiveness of problem-based learning compared to traditional teaching in undergraduate psychiatry.

OBJECTIVES: A change from traditional to problem-based learning (PBL) methods in a psychiatry attachment was evaluated by comparing the learning styles, attitudes to psychiatry and examination performance of 2 cohorts of students. It was hypothesised that the PBL curriculum would result in increased deep learning, decreased surface learning, more favourable attitudes to psychiatry and improved examination performance. It was predicted that students' examination success would be related to the use of deep and strategic learning and favourable attitudes. METHODS: Consecutive cohorts of Year 2 clinical students taught using a traditional psychiatry curriculum (n = 188) and a PBL curriculum (n = 191) were compared. Students completed the Study Process Questionnaire to assess their learning styles and the Attitudes to Psychiatry Scale at the beginning and end of the attachment. Students completed 2 end-of-attachment examinations, a multiple-choice paper and a viva. RESULTS: The PBL curriculum resulted in significantly better examination performance than did the traditional teaching curriculum, both for multiple-choice questions and the viva. No differences in learning styles or attitudes to psychiatry were found between the curricula. Students were significantly more successful in the examinations if they had received the PBL curriculum, were female, and used strategic learning. CONCLUSIONS: Examination performance indicated that the PBL curriculum was more successful than the previous course, but that this improvement was not due to students using more effective learning styles or having more favourable attitudes towards psychiatry. It is possible that students learned more effectively during the teaching sessions in the PBL curriculum, but did not change their preferred learning styles.

Achievement↗

Enrichment enhances the expression of sgk, a glucocorticoid-induced gene, and facilitates spatial learning through glutamate AMPA receptor mediation.

We have previously demonstrated that the serum and glucocorticoid-inducible kinase (sgk) gene plays a causal role in facilitating memory performance in rats. Environment enrichment is known to facilitate spatial learning. We therefore examined the effect of enrichment on sgk expression. We also examined the role of sgk in spatial and nonspatial learning and the regulation of sgk expression by activation of different glutamate receptors. Both real-time polymerase chain reaction and Western blot analyses revealed that enrichment training preferentially increased sgk mRNA and protein levels in the hippocampus. Transfection of sgk mutant DNA to the hippocampal CA1 area markedly impaired spatial learning, fear-conditioning learning and novel object-recognition learning in rats, but enrichment training effectively reversed these learning deficits. Meanwhile, S422A mutant DNA transfection prevented enrichment-induced spatial learning facilitation. In studying glutamate receptor regulation of sgk expression, we found that blockade of N-methyl-d-aspartate (NMDA) receptors in general, and the NR2B subunit in particular both effectively blocked enrichment-induced spatial learning facilitation, but they did not block enrichment-induced sgk expression. Upon various glutamate agonist infusions, only alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) increased sgk mRNA levels significantly in the hippocampus. Furthermore, blockade of AMPA receptors effectively blocked both enrichment-induced spatial learning facilitation and sgk expression. These results indicate that there is a dissociation between NMDA receptor activation and sgk expression. Enrichment enhanced spatial learning through both NMDA and AMPA receptor activation, whereas enrichment-induced sgk expression is specifically mediated through AMPA receptors. These results suggest that sgk could serve as a novel molecular mechanism, in addition to the NMDA receptor NR2B, underlying enrichment-induced learning facilitation.

Age Factors↗

Cellular mechanisms of learning, memory, and information storage.

In Table 1, we summarize what is convincingly demonstrated to date for the major vertebrate and invertebrate model systems attempting to elucidate cellular mechanisms of associative learning. Two major concerns are the adequacy of the behavioral demonstrations and the completeness and extent of the accompanying neurophysiology. In addressing the issue of behavior, it is important to define clearly which criteria are both necessary and sufficient to infer the involvement of an associative-learning process. Similarly, it is also important to distinguish among those primary characteristics of associative learning in general, and those secondary or tertiary features that serve to define various subclasses. In our view, it would be unreasonable to require that any given preparation exhibit all the defining features of classical conditioning, for example, in order to qualify as a "legitimate" instance of associative learning. This is especially true if the goal is to understand the more general, rather than the specific, mechanisms involved in associative learning. Hence, we emphasize the following as primary features of learned behavior: pairing specificity, stimulus specificity, long-term retention (arbitrarily defined as lasting for at least 24 hr), a moderate degree of reversibility by subsequent experience (e.g. extinction), and demonstrations that nonassociative-learning processes cannot account for features a-c. Where appropriate, we also identified other interesting features of the learned behavior. It is apparent from the table that a major unresolved issue for most of the preparations is the extent to which the behavioral changes are exclusively associative. This is no less true for the vertebrate preparations than it is for the invertebrates. The clearest example of an exclusively associative behavioral change is the rabbit NMR. The learning-produced changes in the invertebrate preparations were all shown, to varying degrees, to be pairing specific. Yet a major unresolved issue is the degree to which apparent examples of associative-learning reflect complex interactions among basically nonassociative-learning processes. The core issue is really quite simple: Does the associative training procedure result in the acquisition of new or qualitatively different behavior; and is there a strict requirement for an associative relation? In addressing the adequacy of the neurophysiological analyses, the major issue is that of localization. Logically, there are two components to this.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Human neural learning depends on reward prediction errors in the blocking paradigm.

Learning occurs when an outcome deviates from expectation (prediction error). According to formal learning theory, the defining paradigm demonstrating the role of prediction errors in learning is the blocking test. Here, a novel stimulus is blocked from learning when it is associated with a fully predicted outcome, presumably because the occurrence of the outcome fails to produce a prediction error. We investigated the role of prediction errors in human reward-directed learning using a blocking paradigm and measured brain activation with functional magnetic resonance imaging. Participants showed blocking of behavioral learning with juice rewards as predicted by learning theory. The medial orbitofrontal cortex and the ventral putamen showed significantly lower responses to blocked, compared with nonblocked, reward-predicting stimuli. In reward-predicting control situations, deactivation in orbitofrontal cortex and ventral putamen occurred at the time of unpredicted reward omissions. Responses in discrete parts of orbitofrontal cortex correlated with the degree of behavioral learning during, and after, the learning phase. These data suggest that learning in primary reward structures in the human brain correlates with prediction errors in a manner that complies with principles of formal learning theory.

Adult↗

Contrasting cortical and subcortical activations produced by attentional-set shifting and reversal learning in humans.

Much evidence suggests that lesions of the prefrontal cortex (PFC) produce marked impairments in the ability of subjects to shift cognitive set, as exemplified by performance of the Wisconsin Card Sorting Test (WCST). However, studies with humans and experimental primates have suggested that damage to different regions of PFC induce dissociable impairments in two forms of shift learning implicit in the WCST (that is, extradimensional (ED) shift learning and reversal shift learning), with similar deficits also being apparent after damage to basal ganglia structures, especially the caudate nucleus. In this study, we used the same visual discrimination learning paradigm over multidimensional stimuli, and the H215O positron emission tomography (PET) technique, to examine regional cerebral blood flow (rCBF) changes associated with these subcomponent processes of the WCST. In three conditions, subjects were scanned while acquiring visual discriminations involving either (i) the same stimulus dimension as preceding discriminations (intradimensional (ID) shifts); (ii) different stimulus dimensions from previous discriminations (ED shifts) or (iii) reversed stimulus-reward contingencies (reversal shifts). Additionally, subjects were scanned while responding to already learnt discriminations ('performance baseline'). ED shift learning, relative to ID shift learning, produced activations in prefrontal regions, including left anterior PFC and right dorsolateral PFC (BA 10 and 9⁄46). By contrast, reversal learning, relative to ID shift learning, produced activations of the left caudate nucleus. Additionally, compared to reversal and ID shift learning, ED shift learning was associated with relative deactivations in occipito-temporal pathways (for example, BA 17 and 37). These results confirm that, in the context of visual discrimination learning over multidimensional stimuli, the control of an acquired attentional bias or'set', and the control of previously acquired stimulus-reinforcement associations, activate distinct cortical and subcortical neural stations. Moreover, we propose that the PFC may contribute to the control of attentional-set by modulating attentional processes mediated by occipito-temporal pathways.

Adult↗

Corticohippocampal contributions to spatial and contextual learning.

Spatial and contextual learning are considered to be dependent on the hippocampus, but the extent to which other structures in the medial temporal lobe memory system support these functions is not well understood. This study examined the effects of individual and combined lesions of the perirhinal, postrhinal, and entorhinal cortices on spatial and contextual learning. Lesioned subjects were consistently impaired on measures of contextual fear learning and consistently unimpaired on spatial learning in the Morris water maze. Neurotoxic lesions of perirhinal or postrhinal cortex that were previously shown to impair contextual fear conditioning (Bucci et al., 2000) or contextual discrimination (Bucci et al., 2002) caused little or no impairment in place learning and incidental learning in the water maze. Combined lesions of perirhinal plus lateral entorhinal or postrhinal plus medial entorhinal cortices resulted in deficits in acquisition of contextual discrimination but had no effect on place learning in the water maze. Finally, a parahippocampal lesion comprising combined neurotoxic damage to perirhinal, postrhinal, and entorhinal cortices resulted in profound impairment in acquisition of a standard passive avoidance task but failed to impair place learning. In the same experiment, rats with hippocampal lesions were impaired in spatial navigation. These results indicate that tasks requiring the association between context and an aversive stimulus depend on corticohippocampal circuitry, whereas place learning in the water maze can be accomplished without the full complement of highly processed information from the cortical regions surrounding the hippocampus. The evidence that different brain systems underlie spatial navigation and contextual learning has implications for research on memory when parahippocampal regions are involved.

Animals↗

Effects of errorless and errorful face-name associative learning in moderate to severe dementia.

BACKGROUND AND AIMS: The prevention of errors during learning has been found to be effective in overcoming memory problems in patients with amnesia compared with errorful or trial-and-error learning, possibly as a result of intact implicit memory function. Although errorless learning is a clinically promising technique used in cognitive training settings, to date only a few studies have examined errorless learning in patients with dementia. METHODS: The current study examined errorless and errorful learning using a face-name associative memory task in a group of moderate to severe dementia patients suffering from probable Alzheimer's disease (MMSE < or = 22; n = 10) using a fully counterbalanced within-subject design. RESULTS: Errorless learning had a significantly beneficial effect after two consecutive learning trials (p = 0.01). However, after an unfilled delay of 10 minutes, no significant differences in memory performance were found between errorless and errorful learning. Furthermore, current effects were much smaller compared with previous findings in healthy adults and early-stage dementia patients. CONCLUSIONS: Although errorful learning resulted in better performance in a face-name associative memory task in patients with dementia, this effect was only short-lived. Thus, the beneficial effects of errorless learning are probably not due to intact implicit memory function, but may also be subserved by explicit memory, a memory system that is typically impaired in dementia. Also, the clinical applicability of errorless learning in teaching patients with moderate to severe dementia face-name associations is limited.

Aged↗

Action observation supports effector-dependent learning of finger movement sequences.

Practising a motor skill can result in effector-dependent learning (learning that does not transfer from the set of muscles used in training to a new set of muscles). Proceeding from neurophysiological evidence of motor activation during action observation, this study asked whether observational learning, learning through observation of skilled performance, can also be effector-dependent. Adult human participants observed a model's right hand as the model responded to an eight-item sequence in a serial reaction time (SRT) task. Their sequence learning was then compared in two tests with that of controls who had observed the model's right hand responding to random targets during training. All participants performed the SRT task with their right hand in the first test and with their left hand in the second. Evidence of observational learning was obtained in the right hand test but not in the left hand test. This implies that sequence learning based on observation of right hand performance did not transfer to the left hand, and therefore that observational learning can support effector-dependent learning of finger movement sequences. A second experiment used the same procedure to assess learning by a group of participants who observed a sequence of response locations only. This group did not observe the model's responses. Results suggested that action observation was necessary for the effector-dependent observational learning demonstrated in Experiment 1.

Adult↗

Perceptual or motor learning in SRT tasks with complex sequence structures.

We investigated under which conditions sequence learning in a serial reaction time task can be based on perceptual learning. A replication of the study of Mayr (1996) confirmed perceptual and motor learning when sequences were learned concurrently. However, between-participants manipulations of the motor and perceptual sequences only supported motor learning in cases of more complex deterministic and probabilistic sequence structures. Perceptual learning using a between-participants design could only be established with a simple deterministic sequence structure. The results seem to imply that perceptual learning can be facilitated by a concurrently learned motor sequence. Possibly, concurrent learning releases necessary attentional resources or induces a structured learning condition under which perceptual learning can take place. Alternatively, the underlying mechanism may rely on binding between the perceptual and motor sequences.

Adult↗

Effects of MK-801 on learning and memory as assessed using a novel water maze.

The effects of the NMDA receptor antagonist MK-801 [(+)-10,11-dihydro-5-methyl-5H-dibenzo [a,d]-cyclohepten-5,10 imine hydrogen maleate] on learning and memory were assessed using a water maze. The maze was a traditional type of maze with alleys and choices between various paths, but set inside a pool of water to a height of 25 cm. Different mazes could be configured by altering the arrangement of open vs. closed doors. Both the time required to reach an out-of-the-water exit platform and the errors made during the swim from start to finish were recorded. Learning was assessed during the first 10 to 20 trials in a new maze configuration, while memory was tested after the maze was well learned. Three experiments, some with several phases, were performed. These experiments compared the effects of 0.1 mg/kg of either (+)-MK-801, or (-)-MK-801 vs. saline on learning new maze configurations as well as swimming well-learned mazes. Neither of the MK-801 isomers impaired performance of a previously learned maze. (+)-MK-801 clearly slowed learning of new mazes as measured by both maze completion time and errors committed, while (-)-MK-801 had a significant but smaller effect on learning. Rats given (+)- or (-)-MK-801 (0.1 mg/kg) for 16 days while learning one maze and then challenged to learn a new maze without drug administration performed no differently on the new maze than controls, suggesting that the acute effect of MK-801 on learning is not long lasting.

Animals↗