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Results for “Spatial Learning”

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At least 253 records · Page 14Linked to original sources

PubMed2005

BDNF protects against stress-induced impairments in spatial learning and memory and LTP.

The present study investigated whether infusion of brain-derived neurotrophic factor (BDNF) could ameliorate stress-induced impairments in spatial learning and memory as well as hippocampal long-term potentiation (LTP) of rats. Chronic immobilization stress (2 h/day x 7 days) significantly impaired spatial performance in the Morris water maze, elevated plasma corticosterone, and attenuated LTP in hippocampal slices from these animals as compared with normal control subjects. BDNF was infused into the left hippocampus (0.5 mul/h) for 14 days, beginning 7 days before the stress exposure. The BDNF group was protected from the deleterious effects of stress and performed at a level indistinguishable from normal control animals despite the presence of elevated corticosterone. BDNF alone and sham infusions had no effect on performance or LTP. These results demonstrate that spatial learning and memory, and LTP, a candidate neural substrate of learning and memory, are compromised during chronic stress, and may be protected by BDNF administration.

Animals↗

PubMed2006

NMDA receptor activity in learning spatial procedural strategies I. The influence of hippocampal lesions.

To acquire knowledge about the environment two types of learning are necessary: declarative localizatory learning about where environmental cues and the subject are, and procedural learning about how to explore and move around the environment. Experimental data indicate that hippocampal regions are involved in spatial learning, playing a key role in building spatial cognitive maps. The contribution of hippocampal NMDA receptors to spatial functions is indicated by the disruption of place learning when NMDA long-term potentiation is blocked. Conversely, the hippocampal contribution to the acquisition of procedural strategies is still controversial. Inactivation of the hippocampus by antagonizing the activity of AMPA/kainate receptors results in impaired spatial procedural learning. However, in the presence of a blockade of NMDA long-term potentiation in hippocampal areas it is still possible to learn explorative strategies. To investigate the involvement of the hippocampal NMDA receptors in spatial procedural learning, an NMDA receptor antagonist (CGS 19755) was administered i.p. to unlesioned animals or to animals with total ablation of hippocampal structures that had been tested in the Morris water maze. The CGS administration induced peripheral circling in both unlesioned control animals and in rats with bilateral hippocampal ablation. Conversely, circling was not observed if the drug-treated animals (either unlesioned or lesioned) had been spatially trained before drug administration. These findings indicate that even in the absence of the hippocampal formation the NMDA receptor antagonist found a site of action to influence the acquisition of spatial procedures to search for the platform.

Analysis of Variance↗

PubMed1995

Spatial learning and memory as a function of age in the dog.

Spatial learning and memory were studied in dogs of varying ages and sources. Compared to young dogs, a significantly higher proportion of aged dogs could not acquire a spatial delayed nonmatching-to-sample task. A regression analysis revealed a significant age effect during acquisition. Spatial memory was studied by comparing performance at delay interval of 20, 70, and 110 s. At short delays aged and young dogs were similar; at longer delays, errors increased to a greater extent in old than in young dogs; however this was not statistically significant. It was possible to identify 2 groups of aged animals, age-impaired and age-unimpaired. Several of the dogs were also tested on an object recognition memory task, which was more difficult to learn than the spatial task. The possibility that these findings are confounded by breed differences is considered. Overall, the present results provide further evidence of the value of a canine model of aging.

Aging↗

PubMed1997

Spatial learning deficits in mice with a targeted glucocorticoid receptor gene disruption.

Previous studies in rats using the Morris water maze suggested that the processing of spatial information is modulated by corticosteroid hormones through mineralocorticoid and glucocorticoid receptors in the hippocampus. Mineralocorticoid receptors appear to be involved in the modulation of explorative behaviour, while additional activation of glucocorticoid receptors facilitates the storage of information. In the present study we used the water maze task to examine spatial learning and memory in mice homozygous and heterozygous for a targeted disruption of the glucocorticoid receptor gene. Compared with wild-type controls, homozygous and heterozygous mice were impaired in the processing of spatial but not visual information. Homozygous mutants performed variably during training, without specific platform-directed search strategies. The spatial learning disability was partly compensated for by increased motor activity. The deficits were indicative of a dysfunction of glucocorticoid receptors as well as of mineralocorticoid receptors. Although the heterozygous mice performed similarly to wild-type mice with respect to latency to find the platform, their strategy was more similar to that of the homozygous mice. Glucocorticoid receptor-related long-term spatial memory was impaired. The increased behavioural reactivity of the heterozygous mice in the open field points to a more prominent mineralocorticoid receptor-mediated function. The findings indicate that (i) the glucocorticoid receptor is of critical importance for the control of spatial behavioural functions, and (ii) mineralocorticoid receptor-mediated effects on this behaviour require interaction with functional glucocorticoid receptors. Until the development of site-specific, inducible glucocorticoid receptor mutants, glucocorticoid receptor-knockout mice present the only animal model for the study of corticosteroid-mediated effects in the complete absence of a functional receptor.

Animals↗

PubMed2003

Genetic mapping of variation in spatial learning in the mouse.

Inbred strains of mice are known to differ in their performance in the Morris water maze task, a test of spatial discrimination and place navigation in rodents, but the genetic basis of individual variation in spatial learning is unknown. We have mapped genetic effects that contribute to the difference between two strains, DBA/2 and C57BL6/J, using an F2 intercross and methods to detect quantitative trait loci (QTL). We found two QTL, one on chromosome 4 and one on chromosome 12, that influence behavior in the probe trial of the water maze (genome-wide significance p = 0.017 and 0.015, respectively). By including tests of avoidance conditioning and behavior in a novel environment, we show that the QTL on chromosomes 4 and 12 specifically influence variation in spatial learning. QTL that influence differences in fearful behavior (on chromosomes 1, 3, 7, 15, and 19) operate while mice are trained in the water maze apparatus.

Animals↗

PubMed1989

Long-term acetyl-L-carnitine preserves spatial learning in the senescent rat.

1. Untreated rats of different ages and old rats chronically treated with Acetyl-1-carnitine were subjected to the spatial learning task. 2. For this test, a circular pool filled with milk-opacified water was used. The animals were to reach an escape platform with the aid of visible environmental cues. 3. The experimental results indicated a clear-cut deterioration of the old animal's acquisition ability of a spatial learning task. 4. The long-term treatment (8 months) with Acetyl-1-carnitine was found to antagonize such a deterioration.

Acetylcarnitine↗

PubMed2003

Protective effect of 5-HT1B receptor gene deletion on the age-related decline in spatial learning abilities in mice.

We previously observed that 5 months old serotonin 1B receptor knockout (5-HT1BKO) mice exhibited a facilitation of learning in a long-term spatial memory task in a water maze. In this study, we attempted to assess whether this effect might persist during aging. We compared the performances of young-adult (3 months old) and aged (22 months old) 5-HT1BKO and wild type (WT) mice in the same task. Young-adult and aged KO mice exhibited facilitated acquisition of the reference memory task as compared to their respective WT controls. Generally, the performance of aged KO was similar to that of young-adult WT on the parameters defining performance and motor (swim speed) aspects of the task. During probe trials, all mice presented a spatial selectivity, which was, however, less pronounced in aged than in young-adult WT. No such age-related effect was observed in KO mice. In a massed spatial learning task, aged KO and WT mice globally exhibited the same level of performance. Nevertheless, young-adult and aged KO mice were superior to their WT controls as concerns the working memory component of the task. The data suggest that 5-HT1BKO mice are more resistant than WT to age-related memory decline as concerns both reference/long-term and working/short-term spatial memory.

Aging↗

PubMed2004

Spatial learning deficits after the development of dorsomedial telencephalon lesions in goldfish.

The effects of lesions in the dorsal area of the caudal telencephalon (Carassius auratus) on the retention of spatial learning in goldfish were examined. The experimental paradigm was similar to the dry version of the Morris water maze for rodents. After being trained to reach a criterion, goldfish underwent surgery and were then retrained. In the retraining, dorsomedial lesions resulted in poor performance, while dorsolateral lesions did not. In a landmark task in which a small circular colored cue was set at a food location, dorsomedial lesions did not produce impairment during retraining. These results suggest that dorsomedial lesions selectively caused impairment in the retention of spatial learning.

Analysis of Variance↗

PubMed2005

Spatial learning and long-term potentiation of mutant mice lacking D-amino-acid oxidase.

We evaluated the role of D-amino-acid oxidase on spatial learning and long-term potentiation (LTP) in the hippocampus, since this enzyme metabolizes D-amino-acids, some of which enhance the N-methyl-D-aspartate receptor functions. The Morris water maze learning and the LTP in the CA1 area of the hippocampal slice were observed in wild-type mice and mutant mice lacking D-amino-acid oxidase. The mutant mice showed significantly shorter platform search times in the water maze and significantly larger hippocampal LTPs than the wild-type mice. These results suggest that the abundant D-amino-acids in the mutant mouse brain facilitate hippocampal LTP and spatial learning.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed2006

Spatial learning and goldfish telencephalon NMDA receptors.

Recent results have demonstrated that the mammalian hippocampus and the dorso-lateral telencephalon of ray-finned fishes share functional similarities in relation to spatial memory systems. In the present study, we investigated whether the physiological mechanisms of this hippocampus-dependent spatial memory system were also similar in mammals and ray-finned fishes, and therefore possibly conserved through evolution in vertebrates. In Experiment 1, we studied the effects of the intracranial administration of the noncompetitive NMDA receptor antagonist MK-801 during the acquisition of a spatial task. The results indicated dose-dependent drug-induced impairment of spatial memory. Experiment 2 evaluated if the MK-801 produced disruption of retrieval of a learned spatial response. Data showed that the administration of MK-801 did not impair the retrieval of the information previously stored. The last experiment analyzed the involvement of the telencephalic NMDA receptors in a spatial and in a cue task. Results showed a clear impairment in spatial learning but not in cue learning when NMDA receptors were blocked. As a whole, these results indicate that physiological mechanisms of this hippocampus-dependent system could be a general feature in vertebrate, and therefore phylogenetically conserved.

Animals↗

PubMed1995

Spatial learning impairment in mice infected with Legionella pneumophila or administered exogenous interleukin-1-beta.

The effect of interleukin-1 beta (IL 1 beta) on spatial learning was examined. In one experiment, C57BL/6 mice were given daily injections (100 ng/mouse) of recombinant murine IL1 beta prior to training on the Morris water maze. In another experiment, mice were infected with a sublethal dose of a gram-negative bacterium (Legionella pneumophila; Lp). Mice rendered ill by the infection were given either anti-IL1 beta antibodies (100 micrograms/mouse) or saline and then trained on the water maze. Results indicated that (1) exogenous IL1 beta blocked acquisition of spatial learning, (2) Lp infection attenuated learning on this task, and (3) neutralizing circulating IL1 beta in Lp-infected mice normalized learning despite the continuation of the illness. The data indicate that cognitive impairment may be a component of cytokine-mediated sickness behavior.

Animals↗

PubMed2002

Disruption of estrogen receptor beta gene impairs spatial learning in female mice.

Here we provide the first evidence, to our knowledge, that estradiol (E(2)) affects learning and memory via the newly discovered estrogen receptor beta (ERbeta). In this study, ERbeta knockout (ERbetaKO) and wild-type littermates were tested for spatial learning in the Morris water maze after ovariectomy, appropriate control treatment, or one of two physiological doses of E(2). Regardless of treatment, all wild-type females displayed significant learning. However, ERbetaKOs given the low dose of E(2) were delayed in learning acquisition, and ERbetaKOs administered the higher dose of E(2) failed to learn the task. These data show that ERbeta is required for optimal spatial learning and may have implications for hormone replacement therapy in women.

Animals↗

PubMed1989

Hemicholinium-3 impairs spatial learning and the deficit is reversed by cholinomimetics.

The effects of hemicholinium-3 (HC-3) on spatial discrimination learning were studied. Rats were equipped with indwelling cannulae in the right lateral ventricle and, following recovery, were trained on a two platform spatial discrimination task in a water maze. In this task a visible escape platform remains in a fixed position in the pool during a single training session, whilst the location of an identical "float" (which affords no escape) is randomly varied. For each session the location of the fixed escape platform was changed and the rats were retrained to criterion following pretreatment either with artificial cerebrospinal fluid (CSF) or HC-3 (2.5, 5.0 micrograms/rat/ICV) 1 h before training. Each rat received every treatment according to a latin square design. The results showed that spatial learning was dose dependently impaired by HC-3, choice accuracy being reduced to chance levels by the higher dose. There was no evidence of motoric difficulty, as choice latencies were not significantly increased. Experiments were then conducted to test for reversal of the deficit using a range of psychotropic drugs. Rats were treated with CSF or HC-3 (5 micrograms/rat ICV) 60 min prior to testing and test drugs were injected 15 min before testing. Some doses of physostigmine (46-460 micrograms/kg/SC) and tetrahydroaminoacridine (THA) (2.2-10 mg/kg/SC) reversed the spatial learning deficit. The muscarinic agonists arecoline (0.046-1 mg/kg/SC), aceclidine (1-10 mg/kg/SC), oxotremorine (30-100 micrograms/kg/SC) and RS-86 (0.46, 1.0 microgram/kg/SC) were also effective. Pilocarpine (0.22-2.2 mg/kg/SC) showed marginal activity and isoarecoline (4.6-10 mg/kg/SC) was inactive. Nicotine (0.32, 1, 3.2 mg/kg/SC) and piracetam (10, 30, 100 mg/kg IP) were also inactive. The alpha 2 agonist, clonidine (46, 100 micrograms/kg SC) and the antagonist idazoxan (32, 100 micrograms/kg SC) were also inactive. Learning deficits were not reversed by haloperidol (20, 60 micrograms/kg), amphetamine (0.1, 0.46 mg/kg), the selective 5-HT1A agonist 8-OH-DPAT (30, 100 micrograms/kg) or by the benzodiazapine antagonist ZK-93426 (1, 3.2, 10 mg/kg). The results show that forebrain Ach depletion by HC-3 impairs spatial discrimination learning and these deficits are reversed by cholinesterase inhibitors and some muscarinic receptor agonists. Some degree of pharmacological selectivity is indicated by the failure of a range of other drugs to reverse the impairments.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed2000

Spatial learning and long-term potentiation in the dentate gyrus of the hippocampus in animals developmentally exposed to Aroclor 1254.

Developmental exposure to polychlorinated biphenyls (PCBs) has been associated with cognitive deficits in children. Rodent studies have revealed impairments in learning tasks involving the hippocampus. The present study sought to examine hippocampal synaptic plasticity in the dentate gyrus and spatial learning in animals exposed to PCBs early in development. Pregnant Long-Evans rats were administered either corn oil (control) or 6 mg/kg/day of a commercial PCB mixture, Aroclor 1254 (A1254) by gavage from gestational day (GD) 6 until pups were weaned on postnatal day (PND) 21. Spatial learning was assessed at 3 months of age in male and female offspring using the Morris water maze. Latency to find a hidden platform that remained in the same position over 20 days of testing did not differ between control and PCB-exposed groups. Neither were group differences evident in a repeated acquisition version of the task in which the platform remained in the same position over the 2 daily trials but was moved to a new spatial location each day. Male littermates of animals in the behavioral study were tested electrophysiologically at 5-7 months of age. Field potentials evoked by perforant path stimulation were recorded in the dentate gyrus under urethane anesthesia. Input/output (I/O) functions were assessed by averaging the response evoked in the dentate gyrus to stimulus pulses delivered to the perforant path in an ascending intensity series. Long-term potentiation (LTP) was induced by delivering a series of brief, high-frequency train bursts to the perforant path at increasing stimulus intensities, and I/O functions were reassessed 1 h later. No differences in baseline synaptic population spike (PS) and excitatory postsynaptic potential (EPSP) slope amplitudes were discerned between the groups prior to train delivery. Post-train I/O functions, however, revealed a decrement in the magnitude of evoked LTP in PCB-exposed animals, and an increase in the train intensity required to induce LTP. The observed dissociation between impaired hippocampal plasticity, in the absence of a detectable deficit in performance of a hippocampal-dependent task, may be due to task complexity, the maintenance of some degree of plasticity in the PCB-exposed animals, or the possibility that intact dentate gyrus LTP may not be requisite for water-maze learning.

Animals↗

PubMed1997

WAY 100635, a 5-HT1A receptor antagonist, prevents the impairment of spatial learning caused by intrahippocampal administration of scopolamine or 7-chloro-kynurenic acid.

The effect of WAY 100635, a 5-HT1A receptor antagonist, on the impairment of spatial learning caused by intrahippocampal administration of scopolamine, a cholinergic muscarinic receptor antagonist, or 7-chloro-kynurenic acid, an antagonist at the glycine site associated with the NMDA receptor complex, was studied in a two-platform spatial discrimination task. Scopolamine (4 microg/microl) or 7-chloro-kynurenic acid (3 microg/microl), administered bilaterally into the CA1 region of the dorsal hippocampus 10 min before each training session, impaired choice accuracy with no effect on choice latency and errors of omission. Administered subcutaneously at 1 (but not at 0.3) mg/kg 30 min before each training session, WAY 100635 did not modify the acquisition of spatial learning, but prevented the impairment of choice accuracy caused by intrahippocampal scopolamine or 7-chloro-kynurenic acid. These findings suggest that blockade of 5-HT1A receptors can compensate the loss of cholinergic or NMDA-mediated excitatory input to pyramidal cells in the hippocampus. The mechanisms involved and the importance of these findings for the symptomatic treatment of memory disorders in man are discussed.

Animals↗

PubMed2001

Excitotoxic lesions of the rostral thalamic reticular nucleus do not affect the performance of spatial learning and memory tasks in the rat.

Rats with cytotoxic lesions of the rostral pole of the thalamic reticular nucleus were compared with surgical control animals on a series of spatial learning and memory tests. While evidence was found for an initial, transient impairment on forced-choice alternation in a T-maze, this rapidly disappeared, and overall performance was unaffected. Subsequent experiments found no evidence that lesions of the rostral reticular nucleus affected the acquisition or performance of tests in the radial arm maze and the Morris water maze. Thus, it appears that the rostral pole of the thalamic reticular nucleus often does not play a necessary role in the performance of tests of spatial learning and memory, in spite of its interconnections with other regions that are required for normal spatial memory.

Animals↗

PubMed1996

Spatial learning in a Z-maze by cerebellar mutant mice.

Two types of cerebellar mutant mice (staggerer and lurcher) were evaluated during 5-day acquisition of a spatial learning task in a Z-maze filled with water. Although the number of errors and escape latencies decreased in normal mice, the acquisition of the cerebellar mutants was impaired but not abolished. These results indicate that the cerebellum has a role in spatial learning. Mice with cerebellar dysfunction take a more indirect route toward a goal during the course of swimming, when ataxic symptoms are no longer in evidence.

Animals↗

PubMed1999

Excitotoxic hippocampal lesions disrupt allocentric spatial learning in mice: effects of strain and task demands.

Spatial discrimination of ibotenic acid-lesioned C57BL/6 (B6) and DBA/2 (D2) mice was tested in two-choice water maze and plus maze tasks. B6 but not D2 mice learned the spatial discrimination in the water maze, but strains did not differ in learning a spatial discrimination in the plus maze paradigm. Ibotenic acid lesions of the hippocampus impaired percentage correct choices in the water maze spatial discrimination task in B6 but not in D2 mice, the latter of which may have been due to a floor effect. Furthermore, lesioned mice were more thigmotaxic, the distance travelled until a choice was made was longer and animals made more errors of omission. Despite the poor performance during water maze acquisition, lesioned animals, as well as sham-lesioned D2 mice, eventually acquired some place response in the water maze, as was evident when the location of the platform was reversed. However, hippocampus-lesioned mice of both strains were impaired when tested in the plus maze spatial discrimination task. Thus, ibotenic acid-induced lesions of the hippocampus impair acquisition of spatial discrimination in mice. These deficits were strain-dependent and likely comprise impaired accuracy as well as changes in non-mnemonic types of behaviour. Importantly, lesions in both strains impaired spatial learning, and whether a deficit was seen in mice of the D2 strain seemed to depend on the demands of the task.

Animals↗