Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Spatial Learning”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,747 records · Page 97Linked to original sources
PubMed2006

Expression of p25 impairs contextual learning but not latent inhibition in mice.

The cyclin-dependent kinase 5 activator p25, which is derived from cleavage of p35, is thought to be formed in the brain of patients with Alzheimer's disease and schizophrenia. Female, but not male, transgenic mice expressing low levels of p25 have enhanced hippocampal long-term potentiation and improved spatial learning, raising the hypothesis that p25 may compensate for early learning deficits in Alzheimer's disease in a sex-dependent manner. Here, we show that low levels of p25 do not alter latent inhibition, a phenomenon that is impaired in patients with schizophrenia. We also demonstrate that contextual fear conditioning is impaired in female, but not in male, p25 transgenic mice. Thus, low levels of p25 are not always beneficial for learning as was previously hypothesized.

Analysis of Variance↗
PubMed2003

Differentiating simple versus complex processing speed: influence on new learning and memory performance.

The current study was designed to examine how the construct of human information processing speed is conceptualized and measured, while also examining the influence of information processing speed on higher cognitive processes (i.e., learning). A mixed medical sample of 92 subjects participated in this study. Subjects underwent a broad-based neuropsychological evaluation, including measures of verbal and visuospatial new learning, spatial and verbal working memory, simple reaction time, choice reaction time, and information processing speed. Principal components factor analysis with varimax rotation resulted in a three-factor solution, comprised of: (1) simple speed/reaction time, (2) complex information processing and new learning, and (3) working memory. Notably, this factor solution identified 2 distinct forms of processing speed--simple and complex information processing speeds. In contrast to the abundance of literature grouping these two constructs together under one term (i.e., processing speed), these results indicate simple and complex speed to be distinct constructs assessed with different neuropsychological instruments. While the expected relationship between complex information processing capacities and working memory abilities was evident in this study, information processing speed also showed a significant relationship with new learning ability. The implications of this intriguing relationship are discussed.

Adult↗
PubMed1989

Continuous physostigmine infusion in rats with excitotoxic lesions of the nucleus basalis magnocellularis: effects on performance in the water maze task and cortical cholinergic markers.

Acute peripheral administration of physostigmine inhibits cortical acetylcholinesterase (AChE) for about 1 hr in the rat and improves performance on learning and memory paradigms after excitotoxic lesions of the nucleus basalis magnocellularis (NBM) in rats. This study examined the effects of continuous systemic infusion of physostigmine using osmotic minipumps. One week of continuous physostigmine infusion in normal animals inhibited cortical AChE activity in a dose-dependent manner. Doses causing near maximal (0.06 mg/kg/hr) and ED50 (0.0075 mg/kg/hr) inhibition of cortical AChE activity were used to determine the effects of continuous physostigmine administration on spatial learning in the water maze in rats with bilateral ibotenic acid lesions of the NBM. Physostigmine had no effect on the acquisition of the maze task but prevented the retention deficit measured in untreated NBM-lesioned rats. Physostigmine treatment also improved the search strategy during the spatial probe trial compared to the untreated NBM-lesioned rats. The two doses of physostigmine examined did not produce differential responses on behavioral measures. Although NBM lesions significantly depleted cortical AChE activity, physostigmine treatment reduced the activity further in a dose-dependent manner. Whereas neither the lesion nor the low dose of physostigmine altered cortical receptor binding, the higher dose of physostigmine significantly down-regulated cortical muscarinic receptor binding by 28%. These data demonstrate that enhancement of acetylcholine neurotransmission can improve memory loss and spatial strategy associated with excitotoxic NBM lesions.

Acetylcholinesterase↗
PubMed1999

Anxiety and increased 5-HT1A receptor response in NCAM null mutant mice.

Mice deficient in the neural cell adhesion molecule (NCAM) show behavioral abnormalities as adults, including altered exploratory behavior, deficits in spatial learning, and increased intermale aggression. Here, we report increased anxiety-like behavior of homozygous (NCAM-/-) and heterozygous (NCAM/-) mutant mice in a light/dark avoidance test, independent of genetic background and gender. Anxiety-like behavior was reduced in both NCAM+/+ and NCAM-/- mice by systemic administration of the benzodiazepine agonist diazepam and the 5-HT1A receptor agonists buspirone and 8-OH-DPAT. However, NCAM-/- mice showed anxiolytic-like effects at lower doses of buspirone and 8-OH-DPAT than NCAM+/+ mice. Such increased response to 5-HT1A receptor stimulation suggests a functional change in the serotonergic system of NCAM-/- mice, likely involved in the control of anxiety and aggression. However, 5-HT1A receptor binding and tissue content of serotonin and its metabolite 5-hydroxyindolacetic acid were found unaltered in every brain area of NCAM-/- mice investigated, indicating that expression of 5-HT1A receptors as well as synthesis and release of serotonin are largely unchanged in NCAM-/- mice. We hypothesize a critical involvement of endogenous NCAM in serotonergic transmission via 5-HT1A receptors and inwardly rectifying K+ channels as the respective effector systems.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1994

Effects of a novel compound MCI-225 on impaired learning and memory in rats.

Effects of MCI-225, [4-(2-fluorophenyl)-6-methyl-2-(1-piperazinyl)thieno[2,3-d]pyrimidine monohydrate hydrochloride] on experimental amnesia were studied in rats and compared with those of THA [9-amino-1,2,3,4-tetrahydroacridine]. In the Morris-type water maze task, MCI-225 (1-10 mg/kg, PO) reduced the spatial learning impairment induced by scopolamine (0.5 mg/kg, IP). In a passive avoidance (PA) task, administration of MCI-225 prior to training (1-30 mg/kg, PO) lessened the carbon dioxide (CO2)-induced amnesia in a dose-dependent manner. MCI-225 (1-100 mg/kg) did not affect gross behavior. THA (0.1-3 mg/kg, PO) reduced scopolamine-induced learning deficits in the water maze task, but the effect was not significant. THA (0.3-3 mg/kg, PO) also ameliorated the CO2-induced amnesia, although slightly, in the PA task. THA (10 mg/kg, PO) increased locomotor activity and higher dose of THA (30 mg/kg, PO) induced tremor, hypersalivation, and muscle relaxation. These results suggest that MCI-225 lessens impairments in learning and memory without causing serious behavioral abnormalities.

Animals↗
PubMed2004

Detour behavior in the Quokka (Setonix brachyurus).

Four quokkas (Setonix brachyurus) were tested in their natural environment for the ability to progress around a barrier to a desired goal object (food). Symmetrical and asymmetrical barriers were used with different lengths of side arm. Three quokkas showed significant tendencies to progress either left or right around the barrier, though this laterality declined as the length of the side arm of the barrier was extended. One quokka showed no behavioral laterality and this animal was also the only one to show spatial reasoning (spontaneous selection of the shorter route on first presentation of the asymmetrical barrier) as opposed to spatial learning (progressive improvement in choice of the shorter route with repeated experience).

Animals↗
PubMed2005

Early protein malnutrition changes learning and memory in spaced but not in condensed trials in the Morris water-maze.

Early protein malnutrition induces structural, neurochemical and functional changes in the central nervous system leading to alterations in cognitive and behavioral development of rats. The aim of the present study was to investigate the effects of protein malnutrition during lactation on acquisition and retention of spatial information using different training procedures (spaced x condensed trials). Rats treated with 16% (well-nourished) or 6% (malnourished) protein diets during the lactation phase and nutritionally recovered until 70 days of age were tested in the Morris water-maze in procedures of 1 trial/day (spaced trials), 4, 8, 12 trials/day (intermediate density) and 24 trials/day (condensed trials), completing 24 trials at the end of training. Seven and 28 days after the training the animals were tested again in just one trial to assess long-term memory. The results showed that protein malnutrition caused deficits on the spatial learning and memory in spaced but not in intermediate and condensed trials procedure. Seven and 28 days after the training there was an increase in the latency to find the platform but only malnourished animals submitted to 1 trial/day had significantly higher latency as compared with well-nourished controls. One of the possible hypotheses is that the effect protein malnutrition only in the procedure of spaced trials could be due to deficits in memory consolidation. It is suggested that these deficits can be the result of alterations produced by protein malnutrition in the hippocampal formation or in long-lasting emotional and/or motivational aspects of the rat's behavior.

Aging↗
PubMed2002

Spatial generalization of learning in smooth pursuit eye movements: implications for the coordinate frame and sites of learning.

We have examined the underlying coordinate frame for pursuit learning by testing how broadly learning generalizes to different retinal loci and directions of target motion. Learned changes in pursuit were induced using double steps of target speed. Monkeys tracked a target that stepped obliquely away from the point of fixation, then moved smoothly either leftward or rightward. In each experimental session, we adapted the response to targets moving in one direction across one locus of the visual field by changing target speed during the initial catch-up saccade. Learning occurred in both presaccadic and postsaccadic eye velocity. The changes were specific to the adapted direction and did not generalize to the opposite direction of pursuit. To test the spatial scale of learning, we examined the responses to targets that moved across different parts of the visual field at the same velocity as the learning targets. Learning generalized partially to motion presented at untrained locations in the visual field, even those across the vertical meridian. Experiments with two sets of learning trials showed interference between learning at different sites in the visual field, suggesting that pursuit learning is not capable of spatial specificity. Our findings are consistent with the previous suggestions that pursuit learning is encoded in an intermediate representation that is neither strictly sensory nor strictly motor. Our data add the constraint that the site or sites of pursuit learning must process visual information on a fairly large spatial scale that extends across the horizontal and vertical meridians.

Animals↗
PubMed2004

Characteristics of behavioral abnormalities in alpha1d-adrenoceptors deficient mice.

To investigate the functional role of alpha1d-adrenergic receptor (alpha1d-AR) in the CNS, we have generated mutant mice lacking the alpha1d-AR using a gene targeting approach and examined in detail the effects of alpha1d-AR knockout mice on motor function, sensory function, and learning and memory. alpha1d-AR knockout mice showed better motor coordination at the highest rotating speed of the rotarod performance and stronger muscle tone using the traction meter, but their locomotor activity and swimming ability in the water maze were not affected. In the water maze requiring reference memory, alpha1d-AR knockout mice showed normal spatial learning. In the Y-maze task requiring working memory or attention, alpha1d-AR knockout mice displayed an impaired spontaneous alternation performance. The alpha1d-AR knockout mice tended to display lower levels of acoustic startle responses than the wild-type group at lower pulse intensities, although the acoustic prepulse inhibition was not impaired in the alpha1d-AR knockout mice. Furthermore, the NMDA receptor antagonist, MK-801-induced deficits of acoustic prepulse inhibition were not observed in the alpha1d-AR knockout mice. These results clearly demonstrate that the alpha1d-AR receptor plays an important role in the process of auditory sensory function, attention or working memory rather than reference memory, and the sensorimotor gating deficits induced by the NMDA receptor antagonist.

Acoustic Stimulation↗
PubMed2000

Molecular overexpression of extracellular superoxide dismutase increases the dependency of learning and memory performance on motivational state.

Extracellular superoxide dismutase (EC-SOD) controls the availability of extracellular superoxide and appears to play a role in controlling intercellular signaling. In this role EC-SOD can have potent effects on neurobehavioral function. In previous studies, we have found that either over- or under-expression of EC-SOD in mice significantly impairs spatial learning on the radial-arm maze. In the current study, the neurobehavioral nature of the EC-SOD role in cognitive function was determined. EC-SOD overexpression altered the relationship between both learning and memory with motivational state. Mice were tested in the radial-arm maze under a high motivational state (22-24 hours of food restriction) or a low motivational state (4-6 hours of food restriction). Under a high motivational state, the EC-SOD overexpressing mice were able to learn in the radial-arm maze, albeit at a slightly lower rate than wild-type controls. This contrasts with the failure to learn by EC-SOD overexpressing mice in our previous study conducted with the low motivational state. The change in motivational state did not significantly alter the learning rate of controls. Similarly, during postacquisition memory phase of testing, the EC-SOD overexpressing mice were significantly worse than controls when tested in a low motivational state but not under a high motivation state. As with learning, motivational state did not significantly affect memory performance in controls. This study shows that mice with EC-SOD overexpression are not incapable of learning and memory in the radial-arm maze, but that the mechanisms which allow control animals to perform this task well under low motivational states are deficient in the mice with EC-SOD overexpression.

Animals↗
PubMed2004

Post-treatment, but not pre-treatment, with the selective cyclooxygenase-2 inhibitor celecoxib markedly enhances functional recovery from kainic acid-induced neurodegeneration.

We have investigated the role of inflammation in the excitotoxicity induced by overstimulation of glutamate receptors using kainic acid, an important tool for studying functions related to excitatory amino acid transmission and for producing neuronal death, especially in areas CA1 and CA3 of the hippocampus. We hypothesised that by inhibiting one of the major components of the neuroinflammation response, after kainic acid injection, that there would be less inflammation and therefore a reduction in cell loss, an enhancement of cognitive function (using spatial learning and object exploration tasks) or both. We examined brain-derived neurotrophic factor levels, expecting that there would be a correlation between its level and subsequent recovery. Our results confirmed our hypothesis: the kainic acid injected-rats treated with celecoxib (after kainic injection) performed better in the spatial and non-spatial tasks than the kainic acid-treated group. However, there was not any improvement if celecoxib was given before kainic acid treatment, underlining also the importance of the production of prostaglandin at the beginning of inflammation.

Analysis of Variance↗
PubMed2000

Postnatal intracerebroventricular administrations of NGF alter spatial memory in adulthood.

The present work assessed the effects of intracerebroventricular injections (2x5 mg/2.5 ml) of recombined human nerve growth factor (rhNGF) at postnatal days 2 and 3 upon the development of spatial learning capacities in rats. The treated rats were trained at the age of 22 days to escape onto an invisible platform at a fixed position in space in a Morris navigation task. For half of the subjects, the training position was also cued, a procedure aimed at facilitating escape and reducing attention to the distant spatial cues. At the age of 2 months all the rats were retrained in the same task. Treatment effects were found in both immature and adult rats. The injection of NGF induced a slight alteration of the immature rats' performance. In contrast, a marked impairment of spatial abilities was shown in the 2-month-old rats. The most consistent effects were a significant increase in the escape latency and a decrease bias towards the training platform area during probe trials. The reduction of spatial memory was particularly marked if the subjects had been trained in a cued condition. Taken together, these experiments reveal that an acute pharmacological treatment that leads to transient modifications during early development might induce a behavioural change long after treatment. Thus, the development and the maintenance of an accurate spatial representation are tightly related to the development of brain structures that could be altered by precocious NGF administrations.

Aging↗
PubMed1995

Selective immunotoxic lesions of basal forebrain cholinergic cells: effects on learning and memory in rats.

Male Long-Evans rats were given injections of either 192 IgG-saporin, an apparently selective toxin for basal forebrain cholinergic neurons (LES), or vehicle (CON) into either the medial septum and vertical limb of the diagonal band (MS/VDB) or bilaterally into the nucleus basalis magnocellularis and substantia innominata (nBM/SI). Place discrimination in the Morris water maze assessed spatial learning, and a trial-unique matching-to-place task in the water maze assessed memory for place information over varying delays. MS/VDB-LES and nBM/SI-LES rats were not impaired relative to CON rats in acquisition of the place discrimination, but were mildly impaired relative to CON rats in performance of the memory task even at the shortest delay, suggesting a nonmnemonic deficit. These results contrast with effects of less selective lesions, which have been taken to support a role for basal forebrain cholinergic neurons in learning and memory.

Acetylcholinesterase↗
PubMed2001

Cognitive performances and locomotor activity following dentate granule cell damage in rats: role of lesion extent and type of memory tested.

Intradentate injection of colchicine is one of the techniques used to destroy granule cells. This study compared the behavioral effects of various amounts of colchicine (1.0, 3.0, and 6.0 microg; Col 1, Col 3, and Col 6, respectively) injected into the dentate gyrus of adult Long-Evans male rats. Starting 10 days after lesion surgery, behavioral testing assessed home-cage and open-field locomotion, alternation in a T-maze, water-maze, and radial-maze learning according to protocols placing emphasis on reference, and working memory. All of these tasks are sensitive to hippocampal disruption. Histological verifications showed that the extent of the lesions depends on the dose of colchicine (index of dentate gyrus shrinkage: -33% in Col 1, -54% in Col 3, and -67% in Col 6 rats). Colchicine dose-dependently increased nocturnal home cage activity (an effect found 10 days but not 5 months after surgery), but had no significant effect on open-field locomotion or T-maze alternation. A dose-dependent reference memory impairment was found during the acquisition of spatial navigation in the water maze; Col 3 and Col 6 rats were more impaired than Col 1 rats. During the probe trial (platform removed), control rats spent a longer distance swimming over the platform area than all rats with colchicine lesions. In the working memory version of the test, all rats with colchicine lesions showed significant deficits. The deficits were larger in Col 3 and Col 6 rats compared to Col 1 rats. The lesions had no effect on swimming speed. In the radial-maze test, there was also a dose-dependent working memory impairment. However, reference memory was disrupted in a manner that did not differ among the three groups of lesioned rats. Our data are in line with the view that the dentate gyrus plays an important role in the acquisition of new information and is an integral neural substrate for spatial reference and spatial working memory. They also suggest that damage to granule cells might have more pronounced effects on reference than on working memory in the radial maze. Finally, they demonstrate that part of the variability in the conclusions from previous experiments concerning the role of granule cells in cognitive processes, particularly in spatial learning and memory, may be due to the type of tests used and/or the extent of the damage produced.

Animals↗
PubMed1997

Cognitive impairment in spontaneously hypertensive rats: role of central nicotinic receptors. I.

Both human essential hypertension and genetically induced hypertension in rats have been associated with a range of impairments of cognitive ability. The spontaneous hypertensive rat (SHR) previously has been shown to exhibit a decrease in the expression of brain nicotinic acetylcholine receptors, a factor that could play a role in the impaired ability of this strain in the performance of learning and memory-related tasks. The purpose of this study was to help determine whether task impairment by SHR was related to the reduced expression of central nicotinic acetylcholine receptors. Twelve-week-old SHR were tested in two phases of a water maze (spatial memory) task, and their performance was compared with that of two age-matched normotensive strains, Wistar Kyoto (WKY) and Wistar rats. During Phase 1, SHR exhibited significantly increased latencies to locate a hidden platform as compared with either WKY or Wistar rats. During Phase 2 (subsequent series of trials after a 4-day inter-phase period), where rats were required to find a new platform location, SHR again exhibited significantly impaired performance compared to the normotensive strains. In a single trial passive avoidance paradigm, SHR again displayed significantly reduced avoidance behavior as compared with both WKY and Wistar rats. In consecutive coronal sections, the density of [3H]cytisine binding sites was decreased in SHR by up to 25% in about half of the brain regions examined, with the deficits particularly apparent in cephalic regions. The binding of [125I]alpha-bungarotoxin to brain sections also was decreased in SHR; however, only certain brain areas exhibited significant interstrain differences. These alterations in the expression of putative nicotinic receptor subtypes in SHR were not due to changes in the density of cholinergic neurons since there were no interstrain differences in the binding densities for [3H]vesamicol, which labels the vesicular acetylcholine transporter. Moreover, the magnitude of nicotine-stimulated rubidium efflux from cortical and striatal synaptosomes in vitro was significantly reduced in samples derived from SHR as compared with those from normotensive rats. These results are consistent with the possibility that a reduction in the expression of cortical nicotinic receptors in SHR plays a role in this strain's impaired performance of both spatial and non-spatial learning and memory-related tasks.

Alkaloids↗
PubMed1990

Hippocampal synaptic plasticity and NMDA receptors: a role in information storage?

There has recently been renewed interest in the idea that alterations in synaptic efficacy may be the neural basis of information storage. Particular attention has been focused upon long-term potentiation (LTP), a long-lasting, but experimentally induced synaptic change whose physiological properties point to it being a candidate memory mechanism. However, considerations of storage capacity and the possibility of concomitant activity-dependent synaptic depression make it unlikely that individual learning experiences will give rise to gross changes in field potentials similar to those that occur in LTP, even if learning and LTP utilize common neural mechanisms. One way of investigating the functional significance of LTP is to use selective antagonists of those excitatory amino acid receptors whose activation is essential for its induction. This paper discusses various design requirements for such experiments and reviews work indicating that the N-methyl-D-aspartate receptor antagonist AP5 causes a behaviourally selective learning impairment having certain common features to the behavioural profile seen after hippocampal lesions. Two new studies are described whose results show that AP5 has no effect upon the retrieval of previously established memories, and that the dose-response profile of the impairment of spatial learning occurs across a range of extracellular concentrations in hippocampus for which receptor selectivity exists. These experiments show that activation of NMDA receptors is essential for certain kinds of learning.

Animals↗
PubMedDate not supplied

Hippocampal inactivation enhances taste learning.

Learning tasks are typically thought to be either hippocampal-dependent (impaired by hippocampal lesions) or hippocampal-independent (indifferent to hippocampal lesions). Here, we show that conditioned taste aversion (CTA) learning fits into neither of these categories. Rats were trained to avoid two taste stimuli, one novel and one familiar. Muscimol infused through surgically implanted intracranial cannulae temporarily inactivated the dorsal hippocampus during familiarization, subsequent CTA training, or both. As shown previously, hippocampal inactivation during familiarization enhanced the effect of that familiarization on learning (i.e., hippocampal inactivation enhanced latent inhibition of CTA); more novel and surprising, however, was the finding that hippocampal inactivation during training sessions strongly enhanced CTA learning itself. These phenomena were not caused by specific aspects of our infusion technique--muscimol infusions into the hippocampus during familiarization sessions did not cause CTAs, muscimol infusions into gustatory cortex caused the expected attenuation of CTA, and hippocampal inactivation caused the expected attenuation of spatial learning. Thus, we suggest that hippocampal memory processes interfere with the specific learning mechanisms underlying CTA, and more generally that multiple memory systems do not operate independently.

Animals↗
PubMed1991

Relationship between performance in the Morris water task, visual acuity, and thermoregulatory function in aged F-344 rats.

The present experiments were designed to determine whether the loss of visual acuity and thermoregulatory control in aged rats contributes significantly to age-related deficits in the Morris water task. Relative to 2.5 mo rats, 16-18 mo F-344 rats were found to perform poorly in this spatial learning task. Their performance was also impaired in a test of visual acuity, and they became hypothermic during testing in the Morris water task. Nevertheless, 23 mo F-344 rats still retained a fairly high degree of visual acuity, and reducing the degree of visual acuity required to perform spatial mapping by adding large visual cues in close proximity to the target platform did not improve their performance. However, preventing hypothermia by warming 23 mo rats between trials in the Morris water task did significantly improve performance. These results suggest that age-related deficits in the Morris water task are not due to the loss of visual acuity; but, as a specific measure of cognitive function, performance in the Morris water task may be confounded by the loss of thermoregulatory control.

Aging↗