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Results for “Spatial memory”

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At least 217 records · Page 12Linked to original sources

PubMed2005

Post-training intrahippocampal infusion of nicotine prevents spatial memory retention deficits induced by the cyclo-oxygenase-2-specific inhibitor celecoxib in rats.

Recently, we demonstrated that intrahippocampal infusion of the cyclo-oxygenase (COX)-2-specific inhibitor celecoxib impaired spatial memory retention in the Morris water maze. In the present work, we investigated the effects of nicotine, infused in the rat dorsal hippocampus several minutes after infusion of celecoxib, on memory retention in the Morris water maze. Rats were trained for 3 days; each day included two blocks, and each block contained four trials. Test trials were conducted 48 h after surgery. As expected, bilateral intrahippocampal infusion of celecoxib (19 microg/side; 0.1 m) increased escape latency and travel distance in rats, indicating significant impairment of spatial memory retention. We also examined the effects of bilateral infusion of nicotine (0.5, 1.0 and 2.0 microg/side) on memory retention. Infusion of 1 microg nicotine significantly decreased escape latency and travel distance but not swimming speed, compared with controls, suggesting memory retention enhancement by nicotine at this concentration. In separate experiments, bilateral infusion of nicotine, infused 5 min after 0.1 m (19 microg/side) celecoxib infusion, was associated with escape latency, travel distance and swimming speed profiles very similar to those in control animals. Brain tissue sections from several of these animals were subjected to immunohistochemical staining analysis with anti-COX-2 antibodies. Quantification analysis by optical density measurements showed that the celecoxib infusion reduced the immunoreactivity of COX-2-containing neurons in the CA1 area of the hippocampus compared with controls, although this reduction was not significant. However, infusion of a combination of celecoxib and nicotine significantly increased this immunoreactivity compared with levels in control and celecoxib-infused groups. These results suggest that nicotine prevented or reversed the adverse effects of celecoxib on spatial memory retention and protected or restored the immunostaining pattern of COX-2 neurons in the rat dorsal hippocampus.

Animals↗

PubMed1998

An alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) antagonist and an N-methyl-D-aspartate (NMDA) channel blocker synergistically impair spatial memory in rats.

The interaction of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) antagonist YM90K with the competitive N-methyl-D-aspartate (NMDA) antagonist CGS19755 or with the NMDA channel blocker MK801 on the spatial memory of rats was examined by the 4-arm-baited radial maze task. When administered alone, these drugs had no effect on the spatial memory. The combination of YM90K and MK801 synergistically disrupted working and reference memories, whereas the combination of YM90K and CGS19755 had no effect. These results indicate that the blockade of the AMPA receptor and NMDA channels produces a synergistic impairment of spatial memory and suggest that interaction between the AMPA and NMDA receptors plays a role in cognitive function.

Animals↗

PubMedDate not supplied

Age-related ability of rats kept on a life-long hypocaloric diet in a spatial memory test. Longitudinal observations.

Cognitive behavior was assessed in a test specific for spatial memory, according to a longitudinal experimental model, in populations of 12-, 24- and 30-month-old rats which were fed ad lib either a standard (ST) or a hypocaloric (HY) diet, that had been shown to reduce age-related pathologies and to increase survival. Already at 12 months of age, some cognitive deficits were observed in ST but not in HY rats. When retested 12 and 18 months later, the animals performed better at the beginning of the test than when tested for the first time, indicating that some aspects of previous experience lead to a preservation of spatial memory. Deficits which had been previously observed in 2-year-old groups in a cross-sectional experimental model were not evident this time. Some of the differences between the two diet groups observed 12 months before disappeared. When testing was repeated for the third time at 30 months of age, ST fed rats presented very marked deficits in learning and in memory, which were not seen in the HY group. It thus appears that a dietary regimen in which part of the calorie-rich components, such as lipids and carbohydrates, are replaced with vegetable fibers, retards some of the age-related deteriorations of brain functions.

Aging↗

PubMed2000

Disconnecting hippocampal projections to the anterior thalamus produces deficits on tests of spatial memory in rats.

A disconnection procedure was used to test whether projections from the hippocampus to the anterior thalamic nuclei (AT), via the fimbria-fornix (FX), form functional components of a spatial memory system. The behavioural effects of combined unilateral lesions in the AT and FX were compared when they were either in contralateral hemispheres (AT-FX Contra) or the same hemisphere (AT-FX Ipsi). Other groups received bilateral FX lesions and Sham surgeries. Expt 1 demonstrated that none of these lesions affected performance of an object recognition task, while performance of an object location task, which tests the subjects' preference for an object that has changed location, was impaired in the AT-FX Contra and FX groups. In a T-maze alternation task, however, the FX group was severely impaired while both the AT-FX Ipsi and AT-FX Contra lesion groups showed only a mild impairment. In order to test whether spared crossed projections might support spatial performance in the AT-FX Contra group we then examined the effects of a combined AT-FX Contra lesion coupled with transection of the hippocampal commissure. This combination of lesions produced a severe disruption in spatial memory performance in the water maze, radial arm maze and T-maze, which was significantly greater than that produced by ipsilateral and contralateral AT-FX lesions alone. These results support the notion that disconnection of the AT from their hippocampal inputs produces impairments on a range of spatial memory tasks, but indicate that there are an array of different routes that can subserve this function.

Animals↗

PubMed2005

Posttraining intrahippocampal infusion of a protein kinase AII inhibitor impairs spatial memory retention in rats.

The role of protein kinase AII (PKA II) in spatial memory retention in male rats and its regulation of cholinergic gene expression were explored through the effects of intrahippocampal infusion of H-89, a selective PKA II inhibitor. Alterations in escape latency, travel distance, and swimming speed in a Morris water maze were measured. Animals were trained for 3 days; each day included two blocks, and each block contained four trials. Stereotaxic surgery was employed for the infusions after the last trial on the third day of training, and the animals were tested 48 hr after surgery. Bilateral intrahippocampal infusion of H-89 (2.5 or 5 microM) into the CA1 region generated significant alterations in escape latency and traveled distance but not swimming speed. The response was fairly dose dependent, and the maximal effect was obtained with 5 microM H-89. After behavioral testing, several of the infused animals were transcardially perfused and their brains removed. Brain tissue sections from these rats were subjected to immunohistochemical staining analysis with anticholine acetyltransferase (ChAT) antibodies. These analyses indicated that 5 microM H-89 infusions qualitatively reduced the density of ChAT-containing cholinergic nerve terminals in the dorsal hippocampus. The intrahippocampal infusions with 5 microM H-89 also caused an apparent reduction in the number of ChAT-containing neurons in the medial septum. Our results suggest that PKA II is involved in regulation of cholinergic gene expression and plays an important role in spatial memory retention in rats.

Acetylcholine↗

PubMed2005

Protective effect of melatonin against head trauma-induced hippocampal damage and spatial memory deficits in immature rats.

It is well known that head trauma induces the cognitive dysfunction resulted from hippocampal damage. In the present study, we aimed to demonstrate the effect of melatonin on hippocampal damage and spatial memory deficits in 7-day-old rat pups subjected to contusion injury. Melatonin was injected intraperitoneally at the doses of 5 or 20 mg/kg of body weight immediately after induction of traumatic injury. Hippocampal damage was examined by cresyl violet staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Spatial memory performance was assessed in the Morris water maze. Melatonin significantly attenuated trauma-induced neuronal death in hippocampal CA1, CA3 regions and dentate gyrus, and improved spatial memory deficits, which was equally effective at doses of 5-20 mg/kg. The present results suggest that melatonin is a highly promising agent for preventing the unfavorable outcomes of traumatic brain injury in young children.

Animals↗

PubMed2002

Changes in spatial memory mediated by experimental variation in food supply do not affect hippocampal anatomy in mountain chickadees (Poecile gambeli).

Earlier reports suggested that seasonal variation in food-caching behavior (caching intensity and cache retrieval accuracy) might correlate with morphological changes in the hippocampal formation, a brain structure thought to play a role in remembering cache locations. We demonstrated that changes in cache retrieval accuracy can also be triggered by experimental variation in food supply: captive mountain chickadees (Poecile gambeli) maintained on limited and unpredictable food supply were more accurate at recovering their caches and performed better on spatial memory tests than birds maintained on ad libitum food. In this study, we investigated whether these two treatment groups also differed in the volume and neuron number of the hippocampal formation. If variation in memory for food caches correlates with hippocampal size, then our birds with enhanced cache recovery and spatial memory performance should have larger hippocampal volumes and total neuron numbers. Contrary to this prediction we found no significant differences in volume or total neuron number of the hippocampal formation between the two treatment groups. Our results therefore indicate that changes in food-caching behavior and spatial memory performance, as mediated by experimental variations in food supply, are not necessarily accompanied by morphological changes in volume or neuron number of the hippocampal formation in fully developed, experienced food-caching birds.

Animals↗

PubMed2003

A dual role for poly-ADP-ribosylation in spatial memory acquisition after traumatic brain injury in mice involving NAD+ depletion and ribosylation of 14-3-3gamma.

Poly(ADP-ribose) polymerase-1 (PARP-1) is a homeostatic enzyme that paradoxically contributes to disturbances in spatial memory acquisition after traumatic brain injury (TBI) in transgenic mice, thought to be related to depletion of its substrate nicotinamide adenine dinucleotide (NAD+). In this study, systemic administration of the PARP-1 inhibitor 5-iodo-6-amino-1,2-benzopyrone (INH2BP) after TBI preserved brain NAD+ levels and dose-dependently reduced poly-ADP-ribosylation 24 h after injury. While moderate-dose INH2BP improved spatial memory acquisition after TBI; strikingly, both injured- and sham-mice receiving high-dose INH2BP were unable to learn in the Morris-water maze. Poly-ADP-ribosylated peptides identified using a proteomics approach yielded several proteins potentially associated with memory, including structural proteins (tubulin alpha and beta, gamma-actin, and alpha-internexin neuronal intermediate filament protein) and 14-3-3gamma. Nuclear poly-ADP-ribosylation of 14-3-3gamma was completely inhibited by the dose of INH2BP that produced profound memory disturbances. Thus, partial inhibition of poly-ADP-ribosylation preserves NAD+ and improves functional outcome after TBI, whereas more complete inhibition impairs spatial memory acquisition independent of injury, and is associated with ribosylation of 14-3-3gamma.

14-3-3 Proteins↗

PubMedDate not supplied

CREB antisense oligodeoxynucleotide administration into the dorsal hippocampal CA3 region impairs long- but not short-term spatial memory in mice.

The transcription factor cAMP response-element binding protein (CREB) has a pivotal role in hippocampal synaptic plasticity and hippocampus-dependent long-term memory. We recently demonstrated that the dorsal hippocampal CA3 region is involved in memory consolidation of spatial information tested on a Morris water maze in mice. To test whether activation of CREB in the CA3 region is required for memory consolidation of spatial information, bilaterally cannulated mice were infused 18 h before the beginning of the behavioral training with antisense or control sense CREB oligodeoxynucleotides (ODNs) or buffer. Mice were then subjected to massed training in a spatial version of the water maze and tested for retention 0 or 24 h after the last training session. We showed that CREB antisense ODN-infusion in the CA3 region impaired long-term memory when tested 24 h later but had no effect on spatial acquisition or short-term memory tested immediately after behavioral training. These findings provide evidence that the regionally restricted activation of CREB in the dorsal hippocampal CA3 region is critical for the long-term memory consolidation phase of spatial learning but not for short-term memory.

Animals↗

PubMed2001

A role for the angiotensin AT4 receptor subtype in overcoming scopolamine-induced spatial memory deficits.

There is increasing interest in the role of the brain angiotensin AT4 receptor subtype in cognitive processing. This receptor subtype is activated by angiotensin IV (AngIV), is heavily distributed in the mammalian hippocampus, neocortex, and cerebellum, and has been linked with a learning and memory function. The present investigation utilized intracerebroventricular (i.c.v.)-infused scopolamine hydrobromide (scop), a muscarinic receptor antagonist, to disrupt acquisition of the circular water maze task of spatial memory. All animals received 2 days of training trials (five trials/day) using a visible platform in an effort to preclude subsequent confounding by scopolamine-induced sensory and/or motor impairments. In the first experiment, i.c.v.-infused scopolamine (70 nmol) was followed by 0, 10, 100, or 1000 pmol i.c.v. doses of Nle(1)-AngIV in separate groups of rats. Results indicated that each dose of Nle(1)-AngIV improved the poor acquisition of this task induced by scopolamine treatment. However, the 100- and 1000-pmol doses were most effective with respect to latency and distance to find the submerged pedestal. A second experiment demonstrated that treatment with a specific AT4 receptor antagonist, Nle(1), Leual(3)-AngIV (1000 pmol), blocked the ability of Nle(1)-AngIV (100 pmol) to improve the performance of scopolamine-compromised rats. These results support the notion that hippocampal AT4 receptors are involved in spatial memory processing, and that activation of these binding sites can overcome the disruption of spatial memory accompanying treatment with a muscarinic receptor antagonist.

Analysis of Variance↗

PubMed1992

Intrahippocampal grafts of cholinergic-rich striatal tissue ameliorate spatial memory deficits in rats with fornix lesions.

Previous studies have shown that cholinergic grafts derived from the medial septal nucleus are capable of restoring behavioral function in rats with lesions that sever the cholinergic inputs to the hippocampal formation. In this study, we demonstrate that intrahippocampal grafts of cholinergic-rich striatal tissue also ameliorate spatial memory deficits of rats with fornix lesions. We also found that atropine administration dramatically disrupted spatial navigation performance of rats with striatal grafts and control rats, thus suggesting that the striatal graft effects are mediated by cholinergic mechanisms of action. Measurements of high affinity choline uptake (HACU) and muscarinic receptor binding revealed that intrahippocampal striatal grafts increased HACU and normalized muscarinic receptor binding in animals with fornix lesions. Regression analyses demonstrated significant correlations between the amelioration of spatial memory deficits and hippocampal HACU and receptor binding. We conclude that intrahippocampal grafts of cholinergic-rich striatal tissue can ameliorate spatial memory deficits and that this amelioration is associated with the reinstatement of functional cholinergic terminations.

Animals↗

PubMed1994

Marmoset (Callithrix jacchus jacchus) spatial memory in a foraging task: win-stay versus win-shift strategies.

The spatial memory of common marmosets (Callithrix jacchus jacchus) was explored in 3 experiments with a simulated foraging task. In Experiment 1, individual monkeys foraged among 8 baited food sites. They appeared to use spatial memory to accurately avoid revisiting previously depleted sites. There was no difference in accuracy between the adult monkeys and a juvenile monkey tested on the same task. In Experiment 2, a win-stay paradigm was used. The adult monkey subject very accurately remembered locations that had previously contained food. The monkey tended to visit adjacent correct sites when retrieving food and thus minimized the total distance travelled. In Experiment 3, a win-shift paradigm was used with 2 adult monkeys. Although both monkeys performed at above-chance levels of accuracy on the win-shift task, they made many errors. These results suggest that marmosets may prefer tasks that require a win-stay strategy.

Animals↗

PubMed2000

Frontal-lobe involvement in spatial memory: evidence from PET, fMRI, and lesion studies.

Many studies have identified the prefrontal cortex as the brain area that is critical for spatial memory, both in humans and in other primates. Other studies, however, have failed to establish this relation. Therefore, the aim of this paper was to review the literature regarding the role of the human prefrontal lobe in spatial memory. This was done by examining the evidence obtained from neuropsychological patients and from studies using brain-imaging techniques (PET and fMRI). Evidence supporting the notion that the prefrontal cortex is extensively involved in spatial working memory was found. The majority of these studies, however, suggests that frontal-lobe involvement is not related to the type of material that is being processed (e.g., spatial vs. nonspatial), but to process-specific functions, such as encoding and retrieval. Theoretically, these functions could be linked to the central executive within Baddeley's working-memory model, or to recent theories that emphasize the various processes that play a role in working memory. Also, methodological issues were discussed. Further research is needed to enhance our understanding of the precise interaction of domain-specific and general processes.

Cerebrovascular Circulation↗

PubMed1988

Spatial memory during the tropism of maize (Zea mays L.) coleoptiles.

Photo- or gravitropic stimulation of graminean coleoptiles involves the formation of putative tropistic transverse polarities. It had been postulated that these polarities can be extended by stabilization to developmentally active polarities. Such polarities are known from unicellular spores and zygotes of lower plants and regeneration experiments in dicotyledonous plants. In coleoptiles, photo- or gravitropic stimulation results in stability to counterstimulation of equal strength (with only transient bending in the direction of the second stimulus), as a result of a directional memory, if the time interval between both stimuli exceeds 90 min. This directional memory develops from a labile precursor, which is present from at least 20 min after induction. Once it is stable, spatial memory is conserved for many hours. The formation of spatial memory involves at least one step not present in the common tropistic transduction chain. The spatial expression of memory as curvature is restricted to three distinct responses: (i) curving in the direction of the first stimulus (for time intervals exceeding 90 min); (ii) curving in the direction of the second stimulus (for time intervals shorter than 65 min); and (iii) zero-curvature (for time intervals between 65 and 90 min). This can be interpreted in terms of a stable transverse polarity, which is not identical with the putative tropistic transverse polarity, but might be an extension of it.

Cell Polarity↗

PubMed2004

A role for hippocampal Rho-ROCK pathway in long-term spatial memory.

Morphological changes, including changes in size, shape, and number of synapses, in neurons have been observed in many species and are thought to be critical for long-term memory storage. Actin filaments are intimately involved in neuronal morphology and regulation of their dynamics can influence memory. Rho GTPase plays a prominent role in this process and has been implicated in both pre- and post-synaptic morphological changes. Therefore, we examined the effect of hippocampal manipulation of Rho and ROCK activity on performance in a spatial memory task. Post-training intrahippocampal infusion of an inhibitor of the downstream effector kinase p160ROCK impaired long-term memory. Furthermore, post-training activation of Rho using lysophosphatidic acid (LPA) enhanced long-term spatial memory. This memory enhancing effect of LPA was not mediated via the Erk cascade, as no change in Erk phosphorylation was observed as a result of its administration. Our results demonstrate a role for the Rho-ROCK pathway in hippocampus-dependent spatial memory.

Amides↗

PubMed2004

V1a receptor knockout mice exhibit impairment of spatial memory in an eight-arm radial maze.

In this study, we examined the performance of vasopressin V1a receptor (V1aR) and vasopressin V1b receptor (V1bR) knockout (KO) mice compared to wild-type (WT) mice in an eight-arm radial maze. V1aR KO mice exhibited an impairment of spatial memory in comparison to WT mice. By contrast, we did not observe any significant differences between the V1bR KO mice and the WT mice in the eight-arm radial maze. Moreover, OPC-21268, a selective V1aR antagonist, impaired spatial memory in the eight-arm radial maze in WT mice characterized by an increased number of errors. These results suggest that the V1aR controls spatial memory in mice.

Analysis of Variance↗

PubMed2004

Dissociation of function between the dorsal and the ventral hippocampus in spatial learning abilities of the rat: a within-subject, within-task comparison of reference and working spatial memory.

Lesions restricted to the dorsal, but not the ventral, hippocampus severely impair the formation of spatial memory. This dissociation was first demonstrated using the water maze task. The present study investigated whether the dorsal and the ventral hippocampus are involved differentially in spatial reference and spatial working memory using a four-baited/four-unbaited version of the eight-arm radial maze task. This test allows the concurrent evaluation of reference and working memory with respect to the same set of spatial cues, and thereby enables a within-subjects within-task comparison between the two forms of memory functions. Rats with N-methyl-d-aspartic acid-induced excitotoxic lesions of the dorsal hippocampus, ventral hippocampus or both were compared with sham and unoperated controls. We showed that dorsal lesions were as effective as complete lesions in severely disrupting both reference and working spatial memory, whereas rats with ventral lesions performed at a level comparable with controls. These results lend further support to the existence of a functional dissociation between the dorsal and the ventral hippocampus, with the former being preferentially involved in spatial learning.

Animals↗

PubMed2004

Effect of inhibiting melatonin biosynthesis on spatial memory retention and tau phosphorylation in rat.

We have found recently that melatonin protects SH-SY5Y neuroblastoma cells from calyculin A-induced neurofilament impairment and neurotoxicity. In the present study, we further investigated the in vivo effect of inhibiting melatonin biosynthesis on spatial memory retention and tau phosphorylation in rats and the potential underlying mechanisms by using haloperidol, a specific inhibitor of 5-hydroxyindole-O-methyltransferase, and a key enzyme in melatonin biosynthesis. We have found that injection of haloperidol into the lateral ventricle and into peritoneal cavity compromises spatial memory retention of rats and induces hyperphosphorylation of microtubule-associated protein tau at tau-1 (Ser199/Ser202) and PHF-1 (Ser396/Ser404) epitopes. At mean time, the activity of protein phosphatase-2A (PP-2A), a deficit phosphatase in the Alzheimer's disease brain and superoxide dismutase decreases with an elevated level of malondialdehyde. Supplementation with melatonin by prior injection for 1 wk and reinforcement during the haloperidol administration significantly improves memory retention deficits, arrests tau hyperphosphorylation and oxidative stress, and restores PP-2A activity. These results strongly support the involvement of decreased melatonin in Alzheimer-like spatial memory impairment and tau hyperphosphorylation, and PP-2A may play a role in mediating aberrant melatonin-induced lesions.

Animals↗