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Results for “Spatial Learning”

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At least 451 records · Page 25Linked to original sources

PubMed2003

Loss of spatial learning in a patient with topographical disorientation in new environments.

The case is described of a patient who, following cerebral hypoxia, developed severe difficulty in orienting himself in new environments in the context of a mild global amnesic syndrome. Some episodes he related suggested that his main difficulty was remembering the spatial/directional value of landmarks he recognised. A neuroradiological examination documented severe bilateral atrophy of the hippocampi associated with atrophic changes in the cerebral hemispheres, most marked in the dorsal regions. Neuropsychological and experimental evaluation showed a severe deficit of spatial learning with substantially preserved ability to learn verbal and visual-object information. He was also virtually unable to learn a route in a maze task based exclusively on spatial data, but the availability of visual cues substantially improved his learning. Finally, he performed within normal limits on various tests investigating knowledge acquired premorbidly regarding famous buildings, routes in the town he had been living in since childhood, and geography. Topographical disorientation may be subtended by a specific difficulty in storing the spatial/directional value of visual landmarks in novel environments. The hippocampus appears to be involved in the acquisition of new topographical spatial knowledge.

Adult↗

PubMed2003

The acquisition, retention and reversal of spatial learning in the morris water maze task following withdrawal from an escalating dosage schedule of amphetamine in wistar rats.

Two experiments were carried out to evaluate the effects of amphetamine withdrawal in rats on spatial learning in the water maze. A schedule of repeated d-amphetamine administration lasting for 6 days, with three injections per day (1-5 mg/kg, i.p.), was employed. Experiment 1 demonstrated that amphetamine withdrawal did not impair the acquisition of the water maze task (third to fourth withdrawal days), but amphetamine-withdrawn rats made more target-zone visits and reached the former location of the platform quicker than controls during the probe test (fifth withdrawal day). In experiment 2, retention of the location of the escape platform was assessed in animals having been pre-trained on the water maze task before treatment. On the third withdrawal day, retention of the former platform location was assessed in a probe test. Retention was only clearly seen in the measure of target zone visits, and performance did not differ between groups. Next, the animals were trained to escape to a new location in the water maze on withdrawal days 4-5. A reversal effect could be discerned across the first four trials, as evident by the animals' tendency to search in the former target quadrant. This interfered with the new learning, but amphetamine-withdrawn animals appeared to overcome it more rapidly than saline-treated controls. This finding is consistent with the view that amphetamine withdrawal can enhance behavioural switching, which could be expressed as a reduction of proactive interference during learning; and, it is in line with our previous finding that latent inhibition is also attenuated during amphetamine withdrawal.

Amphetamine↗

PubMed2001

Stress, hippocampal plasticity, and spatial learning.

During the last two decades numerous studies have been conducted in an attempt to correlate the mechanisms of long-term potentiation (LTP) of hippocampal synaptic transmission with those required for spatial memory formation in the hippocampus. Because stressful events block the induction of hippocampal LTP, it has been suggested that deficits in spatial learning following stress may be related to suppression of LTP-like phenomena in the hippocampus. Here I review these studies and discuss them in light of the emerging view that stress may induce changes in thresholds for synaptic plasticity necessary for both LTP induction and spatial memory formation. This phenomenon, known as metaplasticity, may involve a glucocorticoid modulation of calcium homeostasis.

Animals↗

PubMed2005

Spatial learning of mice lacking a neuron-specific epidermal growth factor family protein, NELL2.

NELL2 is a neuron-specific thrombospondin-1-like extracellular protein containing six epidermal growth factor-like domains. We previously disrupted the NELL2 gene in mice by gene targeting and showed that long-term potentiation is enhanced in vivo in the dentate gyrus of NELL2-deficient mice. To further elucidate the physiological roles of NELL2, we performed a behavioral characterization of NELL2(-/-) and their heterozygous control mice. NELL2-deficient mice exhibited learning impairment in the Morris water maze task. However, we observed no difference in passive avoidance learning between NELL2(-/-) and NELL2(+/-) mice. These observations suggest that NELL2 plays an important role in hippocampus-dependent spatial learning and that emotional learning does not depend critically on NELL2.

Animals↗

PubMed1993

Neuropeptide FF (FLQPQRFamide) and IgG from neuropeptide FF antiserum affect spatial learning in mice.

There is evidence indicating that the mammalian octapeptide FLQPQRFamide (F8Fa or neuropeptide FF, NPFF) is an endogenous modulator ('anti-opioid') of opioid systems. There is also substantial evidence implicating opioid systems in the mediation of spatial learning and memory. In the present study determinations were made of the effects of NPFF and IgG from antiserum against NPFF on the spatial performance of male mice in a water maze task, whereby over one day in six blocks of four trials the animals had to acquire the location of a submerged hidden platform using distal visual cues. Pretraining intracerebroventricular (i.c.v.) injection of NPFF-IgG, impaired spatial acquisition and retention, while i.c.v. administration of 1.0 microgram of NPFF marginally improved, and 10 micrograms of NPFF significantly reduced spatial acquisition. These results suggest that NPFF may have a modulatory influence on spatial acquisition.

Amino Acid Sequence↗

PubMed2004

Effects of age and spatial learning on adenylyl cyclase mRNA expression in the mouse hippocampus.

Adenylyl cyclase (AC) subtypes have been implicated in memory processes and synaptic plasticity. In the present study, the effects of aging and learning on Ca2+/calmodulin-stimulable AC1, Ca2+-insensitive AC2 and Ca2+/calcineurin-inhibited AC9 mRNA level were compared in the dorsal hippocampus of young-adult and aged C57BL/6 mice using in situ hybridization. Both AC1 and AC9 mRNA expression were downregulated in aged hippocampus, whereas AC2 mRNA remained unchanged, suggesting differential sensitivities to the aging process. We next examined AC mRNA expression in the hippocampus after spatial learning in the Morris water maze. Acquisition of the spatial task was associated with an increase of AC1 and AC9 mRNA levels in both young-adult and aged groups, suggesting that Ca2+-sensitive ACs are oppositely regulated by aging and learning. However, aged-trained mice had reduced AC1 and AC9, but greater AC2, mRNA levels relative to young-trained mice and age-related learning impairments were correlated with reduced AC1 expression in area CA1. We suggest that reduced levels of hippocampal AC1 mRNA may greatly contribute to age-related defects in spatial memory.

Adenylyl Cyclases↗

PubMed1995

Low-dose challenge by the NMDA receptor antagonist dizocilpine exacerbates the spatial learning deficit in entorhinal cortex-lesioned rats.

We investigated the effects of a bilateral quinolinic acid lesion of the medial entorhinal cortex (EC) on acquisition of a spatial learning task. During reversal of the same task, we challenged the animals by the N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine (MK-801). Training took postoperatively place in an eight-arm radial maze in which four of eight arms were baited. In the acquisition phase (ten blocks of five trials) of the test, EC-lesioned animals showed a working (WM) and a reference memory (RM) deficit. The WM deficit was prominent at the beginning and fully compensated at the end of the acquisition phase. The RM deficit became more evident during the course of the experiment. In the reversal learning phase (seven blocks of five trials), the formerly unbaited arms were baited and half of the control and lesioned animals were challenged by a low dose of dizocilpine (0.04 mg/kg i.p.) before training. Only lesioned and additionally dizocilpine-treated animals showed a WM deficit that was again compensated and a RM deficit that was stronger at the end of the test. In summary, quinolinic acid lesion of the medial EC induces both WM and RM deficits in rats. The WM deficit is rapidly compensated. Enhancement of these deficits by challenge with dizocilpine in the reversal learning phase suggests that the NMDA receptor system was rendered more sensitive by this type of lesion.

Animals↗

PubMed2004

Estrogen treatment improves spatial learning in APP + PS1 mice but does not affect beta amyloid accumulation and plaque formation.

We investigated the effects of ovariectomy (OVX) and 17 beta-estradiol (0.18 mg per pellet) treatment on spatial learning and memory, hippocampal beta amyloid (A beta) levels, and amyloid plaque counts in double transgenic mice (A/P) carrying mutated amyloid precursor protein (APPswe) and presenilin-1 (PS1-A246E). After OVX at 3 months of age, the mice received estrogen treatment for the last 3 months of their lifetime before they were killed at 6, 9, or 12 months of age. Estrogen treatment in A/P OVX mice increased the number of correct choices in a position discrimination task in the T-maze, and slightly improved their performance in a win-stay task (1/8 arms baited) in the radial arm maze (RAM). However, estrogen treatment did not reverse the A beta-dependent cognitive deficits of A/P mice in the water maze (WM) spatial navigation task. Furthermore, ovariectomy or estrogen treatment in OVX and sham-operated A/P mice had no effect on hippocampal amyloid accumulation. These results show that the estrogen treatment in a transgenic mouse model of Alzheimer's disease (AD) improves performance in the same learning and memory tasks as in the normal C57BL/6J mice. However, the estrogen effects in these mice appeared to be unrelated to A beta-induced cognitive deficits. Our results do not support the idea that estrogen treatment decreases the risk or alleviates the symptoms of Alzheimer's disease by inhibiting the accumulation of A beta or formation of amyloid plaques.

Age Factors↗

PubMed2005

Impairment of hippocampal long-term depression and defective spatial learning and memory in p35 mice.

Cdk5 (cyclin-dependent kinase 5) activity is dependent upon association with one of two neuron-specific activators, p35 or p39. Genetic deletion of Cdk5 causes perinatal lethality with severe defects in corticogenesis and neuronal positioning. p35(-/-) mice are viable with milder histological abnormalities. Although substantial evidence implicates Cdk5 in synaptic plasticity, its role in learning and memory has not been evaluated using mutant mouse models. We report here that p35(-/-) mice have deficiencies in spatial learning and memory. Close examination of hippocampal circuitry revealed subtle histological defects in CA1 pyramidal cells. Furthermore, p35(-/-) mice exhibit impaired long-term depression and depotentiation of long-term potentiation in the Schaeffer collateral CA1 pathway. Moreover, the Cdk5-dependent phosphorylation state of protein phosphatase inhibitor-1 was increased in 4-week-old mice due to increased levels of p39, which co-localized with inhibitor-1 and Cdk5 in the cytoplasm. These results demonstrate that p35-dependent Cdk5 activity is important to learning and synaptic plasticity. Deletion of p35 may shift the substrate specificity of Cdk5 due to compensatory expression of p39.

Amino Acid Sequence↗

PubMed1997

Intact spatial learning and memory in transgenic mice with reduced BDNF.

Long-term potentiation (LTP) in hippocampal CA1 pyramidal cells is considered to be a cellular analogue of learning and may be useful in studying the molecular foundations of learning and memory. Because brain-derived neurotrophic factor (BDNF) had been shown to have a role in activity-dependent neuroplasticity in the hippocampus we studied spatial learning in mice with BDNF deficiency produced by gene-targeted mutation. Heterozygous BDNF knockout mice reportedly underexpress BDNF and have reduced LTP, but their spatial memory and search strategy assessed with Morris water maze (distally cued version) as well as their performance on the elevated plus maze were indistinguishable from that of controls. This indicates that extrapolation from LTP in a single brain structure to complex behaviours such as learning and memory may not be justified.

Analysis of Variance↗

PubMed1994

Cholesterol treatment facilitates spatial learning performance in DBA/2Ibg mice.

DBA/2Ibg mice were treated with cholesterol pellets for 11 days. On the seventh day after treatment, animals began 5 consecutive days of training on the spatial form of Morris water task, followed on the third and fourth days by a probe trial, and random platform training on the fifth day. DBA mice with cholesterol pellets exhibited enhanced performance compared to DBA mice that underwent a sham surgery. Our results suggest that subchronic treatment with the steroid hormone precursor, cholesterol, enhances spatial learning performance in DBA mice.

Animals↗

PubMed1995

Exposure to stable flies reduces spatial learning in mice: involvement of endogenous opioid systems.

Biting flies influence both the physiology and behaviour of domestic and wild animals. This study demonstrates that relatively brief (60 min) exposure to stable flies, Stomoxys calcitrans (L.), affects the spatial abilities of male mice. Stable fly exposure resulted in poorer subsequent performance in a water maze task in which individual mice had to learn the spatial location of a submerged hidden platform using extramaze visual cues. Determinations of spatial acquisition and retention were made with mice that had been previously exposed for 60 min to either stable flies or house flies, Musca domestica (L.). Mice exposed to stable flies displayed over one day of testing (six blocks or sets of four trials) significantly poorer acquisition and retention of the water maze task than either mice that had been exposed to house flies or fly-naive mice. This attenuation of spatial learning occurred in the absence of any evident sensorimotor or motivational impairments. The reduction in spatial abilities involved endogenous opioid systems, as the decreased performance resulting from stable fly exposure was blocked by pre-treatment with the prototypic opiate antagonist, naltrexone. These results indicate that relatively brief exposure to biting flies can lead to a decrease in spatial abilities which is associated with enhanced endogenous opioid activity. These results support the involvement of endogenous opioid systems in the mediation of the behavioural and physiological effects of biting fly exposure. They further suggest that decreases in spatial abilities and performance may be part of the behavioural consequences of biting fly exposure in domestic and wild animals.

Animals↗

PubMed2005

Exploratory activity and spatial learning in 12-month-old APP(695)SWE/co+PS1/DeltaE9 mice with amyloid plaques.

APP(695)SWE/co+PS1/DeltaE9 mice with Abeta plaques in neocortex and hippocampus were evaluated in tests of exploratory activity and spatial learning. On the initial testing day, 12-month-old APP(695)SWE/co+PS1/DeltaE9 mice spent more time than non-transgenic controls in the open arms of the elevated plus-maze. The bigenic group also travelled farther in the central region of the open-field without spending more time there. Only the bigenic group alternated above chance in the T-maze. In the Morris water maze, APP(695)SWE/co+PS1/DeltaE9 mice were impaired during acquisition of the hidden platform sub-task and the probe trial but not in the visible platform test. These results indicate a selective spatial deficit and disinhibitory tendencies in a mouse model with amyloid pathology.

Amyloid beta-Protein Precursor↗

PubMed2006

Interleukin-10 (IL-10) but not Lipopolysaccharide (LPS) produces increased motor activity and abnormal exploratory patterns while impairing spatial learning in Balb/c mice.

Lipopolysaccharide (LPS) is a potent endotoxin, which produces "sickness behaviours" including loss of weight, loss of interest in food and decreased exploration. LPS has also been shown in some studies to cause deficits in various learning and memory abilities, while in others these LPS-induced learning impairments have been attributed to performance-related deficits rather than learning deficits per se. Here, we use the novelty-preference paradigm, a task that minimises performance-related factors such as motivation, in an attempt to extract and examine the effects of LPS on spatial learning. In addition, some studies have indicated that the anti-inflammatory cytokine Interleukin-10 (IL-10) can alleviate some of the symptoms induced by LPS. Here, we also examine the effect of IL-10 on feeding, motor and learning behaviours. We demonstrate that a single injection of LPS does produce a lack of interest in food and weight loss; LPS, however, does not impair habituation in the novelty-preference paradigm. Furthermore, co-injection of IL-10 with LPS does not attenuate the LPS-induced effects of weight loss and lack of food intake. Interestingly, a single injection of IL-10 produces abnormal patterns of exploration, a general increase in activity and abnormal patterns of habituation.

Analysis of Variance↗

PubMed1996

Differential effects of anterior and posterior insular cortex lesions on the acquisition of conditioned taste aversion and spatial learning.

In this study, we evaluated the effects of NMDA-induced lesions in different sites of the insular cortex of the rat on the acquisition of conditioned taste aversion and spatial learning in the Morris water maze. The lesions were produced by bilateral microinjections of NMDA in the insular cortex at +3.7 mm (Anterior group), +1.7 mm (Central group), and -0.3 mm (Posterior group) anteroposterior from bregma. The results showed that the central and posterior, but not the anterior, lesions disrupted the acquisition of water maze learning as measured by the high latency to reach the target. In contrast, the conditioned taste aversion learning was disrupted by lesions in the central but not in the anterior or posterior insular cortex. These data confirm functional heterogeneity of the insular cortex and demonstrate that the more caudal parts are only necessary for acquisition of the water maze task, while the central insular cortex is crucial for the acquisition of both the conditioned taste aversion learning and the Morris water maze.

Animals↗

PubMed2002

Hippocampus lesions impair landmark array spatial learning in homing pigeons: a laboratory study.

Hippocampal (HF)-lesioned pigeons display impaired homing ability when flying over familiar terrain, where they are presumably relying on a map-like representation of familiar landmarks to navigate. However, research carried out in the field precludes a direct test of whether hippocampal lesions compromise the ability of homing pigeons to navigate by familiar landmarks. To examine more thoroughly the relationship between hippocampus and landmark spatial learning, control, neostriatum-lesioned, and HF-lesioned homing pigeons were trained on two open field, laboratory, conditional discrimination tasks. One was a visual landmark array task, and the other was a room color discrimination task. For the tasks, the correct of three differently colored food bowls was determined by the spatial relationship among a group of five landmarks and room color, respectively. Intact control birds successfully learned both tasks, while neostriatum-lesioned birds successfully learned the landmark array task-the only task on which they were trained. By contrast, HF-lesioned birds successfully learned the room color task but were unable to learn the landmark array task. The data support the hypothesis that homing performance deficits observed in the field following hippocampal lesions are in part a consequence of an impairment in the ability of lesioned pigeons to use familiar visual landmarks for navigation.

Animals↗

PubMed2006

Repeated withdrawal from ethanol spares contextual fear conditioning and spatial learning but impairs negative patterning and induces over-responding: evidence for effect on frontal cortical but not hippocampal function?

Repeated exposure of rats to withdrawal from chronic ethanol reduces hippocampal long-term potentiation and gives rise to epileptiform-like activity in hippocampus. We investigated whether such withdrawal experience also affects learning in tasks thought to be sensitive to hippocampal damage. Rats fed an ethanol-containing diet for 24 days with two intermediate 3-day withdrawal episodes, resulting in intakes of 13-14 g/kg ethanol per day, showed impaired negative patterning discrimination compared with controls and animals that had continuous 24-day ethanol treatment, but did not differ from these animals in the degree of contextual freezing 24 h after training or in spatial learning in the Barnes maze. Repeatedly withdrawn animals also showed increased numbers of responses in the period immediately before reinforcement became available in an operant task employing a fixed-interval schedule although overall temporal organization of responding was unimpaired. Thus, in our model of repeated withdrawal from ethanol, previously observed changes in hippocampal function did not manifest at the behavioural level in the tests employed. The deficit seen after repeated withdrawal in the negative patterning discrimination and over-responding in the fixed-interval paradigm might be related to the changes in the functioning of the cortex after withdrawal.

Animals↗

PubMed2004

Reduction in size of perforated postsynaptic densities in hippocampal axospinous synapses and age-related spatial learning impairments.

A central problem in the neurobiology of normal aging is why learning is preserved in some aged individuals yet impaired in others. To investigate this issue, we examined whether age-related deficits in spatial learning are associated with a reduction in postsynaptic density (PSD) area in hippocampal excitatory synapses (i.e., with a structural modification that is likely to have a deleterious effect on synaptic function). A hippocampus-dependent version of the Morris water maze task was used to separate Long-Evans male rats into young adult, aged learning-unimpaired, and equally aged learning-impaired groups. Axospinous synapses from the CA1 stratum radiatum were analyzed using systematic random sampling and serial section analyses. We report that aged learning-impaired rats exhibit a marked ( approximately 30%) and significant reduction in PSD area, whereas aged learning-unimpaired rats do not. The observed structural alteration involves a substantial proportion of perforated synapses but is not observed in nonperforated synapses. These findings support the notion that many hippocampal perforated synapses become less efficient in aged learning-impaired rats, which may contribute to cognitive decline during normal aging.

Aging↗