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Results for “Spatial memory”

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At least 505 records · Page 28Linked to original sources

PubMed2002

Impairment of adenylyl cyclase and of spatial memory function after microsphere embolism in rats.

The purpose of the present study was to characterize alterations in the adenylyl cyclase (AC), cyclic adenosine 3',5'-monophosphate (cAMP), and spatial memory function after sustained cerebral ischemia. Sustained cerebral ischemia was induced by injection of 900 microspheres (48 microm in diameter) into the right (ipsilateral) hemisphere of rats. Alterations in the AC and cAMP in the cerebral cortex and hippocampus were examined up to 7 days after the embolism. A decrease in the cAMP content was seen in the ipsilateral hemisphere throughout the experiment. Microsphere embolism (ME) decreased the activity of Ca(2+)/calmodulin (CaM)-sensitive AC in the ipsilateral hemisphere throughout the experiment, whereas the basal and 5'-guanylyl imidodiphosphate (Gpp(NH)p)-sensitive AC activities were not altered. Immunoblotting analysis of AC subtypes with specific antibodies showed a decrease in the immunoreactivity of AC-I in the ipsilateral hemisphere during these periods. No significant differences in the immunoreactivity of AC-V/VI and AC-VIII were observed after ME. The levels of GTP-binding proteins Galpha(s), Galpha(i), and Gbetawere unchanged. Furthermore, microsphere-embolized rats showed prolongation of the escape latency in the water maze task determined on the seventh to ninth day after the operation. These results suggest that sustained cerebral ischemia may induce the impairment of the AC, particularly a selective reduction in the AC-I level and activity, coupled with the decrease in cAMP content. This reduction may play an appreciable role in the disturbance in cAMP-mediated signal transduction system, possibly leading to learning and memory dysfunction.

Adenylyl Cyclases↗

PubMed1992

Amygdala kindling-induced seizures selectively impair spatial memory. 2. Effects on hippocampal neuronal and glial muscarinic acetylcholine receptor.

The muscarinic acetylcholine receptor is linked via hydrolysis of phosphoinositides to the protein kinase C pathway. In a preceding paper (Beldhuis, H. J. A., H. G. J. Everts, E. A. Vander Zee, P. G. M. Luiten, and B. Bohus (1992) Amygdala kindling-induced seizures selectively impair spatial memory. 1. Behavioral characteristics and effects on hippocampal neuronal protein kinase C isoforms. Hippocampus 2:397-410), the role of different isoforms of protein kinase C in neurobiological processes associated with plasticity was studied using both a spatial learning paradigm and amygdala kindling in the rat. This study extended the findings on protein kinase C activity to the level of the muscarinic acetylcholine receptor. Rats were trained in a spatial learning paradigm and kindled simultaneously in the amygdala to develop generalized motor convulsions. Control rats were trained only in the spatial learning paradigm to acquire stable working and reference memory performance. Alteration in the expression of the muscarinic acetylcholine receptor was investigated using a monoclonal antibody to muscarinic acetylcholine receptor proteins. Trained control rats that were exposed repeatedly to the spatial learning paradigm showed an increase in immunoreactivity for the muscarinic acetylcholine receptor located in the same hippocampal regions in which the protein kinase C activity was increased. In fully kindled rats, however, this increase located in principal neurons was absent, whereas expression of muscarinic acetylcholine receptor proteins was increased in hippocampal astrocytes. Moreover, fully kindled rats showed an impairment in reference memory performance as compared to trained control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗

PubMed2007

Combination of rimonabant and donepezil prolongs spatial memory duration.

The observations that the cannabinoid(1)(CB(1)) receptor antagonist/inverse agonist, rimonabant, and the selective noncompetitive inhibitor of acetylcholinesterase (AChE), donepezil, improve performance in a variety of animal memory models, suggest that these neurochemical systems play integral roles in cognition. The present study tested whether each of these agents administered alone or in combination will prolong the duration of spatial memory. Rats were trained in a two-phase radial-arm maze procedure, consisting of acquisition and retrieval tests, which were separated by an 18 h delay. Each drug was administered 30 min before the acquisition phase, immediately after the acquisition phase, or 30 min before the retrieval test to assess acquisition/consolidation, consolidation, and retrieval mnemonic processes, respectively. Rimonabant or donepezil administered before the acquisition phase, but not immediately after acquisition or before retrieval, led to a significant decrease in the number of errors committed during the retrieval test. Combined administration of subthreshold doses of rimonabant and donepezil that had no discernable effects on performance when given alone, enhanced memory. These results taken together demonstrate that the delay radial-arm maze task is sufficiently sensitive to detect memory enhancing effects of these drugs. Moreover, these findings suggest that combined administration of subthreshold doses of rimonabant and donepezil can improve memory and may represent a novel approach to treat cognitive deficits associated with neurodegenerative disorders.

Analysis of Variance↗

PubMed2005

Bilateral injection of isoproterenol into hippocampus induces Alzheimer-like hyperphosphorylation of tau and spatial memory deficit in rat.

The abnormal hyperphosphorylation of tau protein is one of the hallmarks of Alzheimer disease and other tauopathies; as yet the exact role of various tau kinases in this pathology is not fully understood. Here, we show that injection of isoproterenol, an activator of cAMP-dependent kinase (PKA), into rat hippocampus bilaterally results in the activation of PKA, calcium/calmodulin-dependent kinase II and cyclin-dependent kinase-5, inhibition of protein phosphatase-2A, hyperphosphorylation of tau at several Alzheimer-like epitopes and a disturbance of spatial memory retention 48 h after the drug injection. These findings suggest the involvement of PKA and PKA-mediated signaling pathway in the Alzheimer-like tau hyperphosphorylation and memory impairment.

Alzheimer Disease↗

PubMed1999

Adaptation of the circular platform spatial memory task for mice: use in detecting cognitive impairment in the APP(SW) transgenic mouse model for Alzheimer's disease.

A methodology is described for use of a 16-hole circular platform task to test spatial memory in mice. Both bright light and a fan were used to motivate mice to escape the platform surface through a single hole containing an attached escape box. For each daily trial, three correlated measures (escape latency, number of errors, and error rating) comprehensively evaluated cognitive performance. In an initial study, the 'spatial' nature of this task was demonstrated by the much poorer performance of non-transgenic mice when visual cues are removed. Behavioral sensitivity of the circular platform task was then shown through its ability to discern cognitive impairment in 7-month-old transgenic mice, carrying the mutant APP(SW) gene for early-onset Alzheimer's disease in humans, from non-transgenic litter-mates. Since there are currently only a few tasks available to definitively test cognitive performance in mice, the circular platform task offers a versatile, multiple-measure option with numerous advantages. Particularly in view of the increasing number of genetically manipulated mouse models being produced, the circular platform task should be most useful in providing a sensitive evaluation of cognition in mice.

Alzheimer Disease↗

PubMed2002

Selective impairments in spatial memory after ischaemic stroke.

There is evidence that object-location memory consists of three separate processes, that is, positional memory, binding of objects to locations, and a possible integration mechanism. A group of 26 patients with lesions following ischaemic stroke was studied to find evidence for selective impairments in these three processes using displays with pictures of everyday objects on different locations. Moreover, object-recognition memory and visuospatial construction was assessed. The Corsi Block-Tapping Task and Oxford Stylus Maze Test were included as standard spatial-memory tests. The results showed that of these 26 patients, 8 patients had selective impairments in the aforementioned object-location memory task conditions (both after immediate and delayed testing). These data further support the existence of separate cognitive processes within memory for object locations that can be selectively affected by cerebral dysfunction.

Adult↗

PubMed1994

Characteristics of spatial memory span: is there an analogy to the word length effect, based on movement time?

In studies of verbal short-term memory it has been shown that the length of words to be remembered affects the size of memory span. This word-length effect is attributed to relationships between the rate of rehearsal of verbal material and the time it takes to speak the words being rehearsed. For spatial memory span there may also be an internal rehearsal system linked to overt responding, and if there is a strong analogy to be drawn between the verbal and spatial domains then movement time between spatial targets should predict the number of spatial locations that can be recalled. In the experiments reported here the time taken to move between spatial targets is varied by altering the size of targets and the distance between them. No difference between span performance on a nine-block spatial span task were found, either on immediate recall or on recall after an interval. When recall is of items from an array of 27, grouped in nine sets of three, with only one location in any set being presented on any trial, there is an effect of display size. This effect is consonant with the argument that movement time is related to spatial rehearsal, but other explanations are also possible. However, if recall in this task is scored over the nine sets rather than over the 27 items, then there is no difference between the displays. The results indicate that performance on the normal nine-block spatial-span task cannot be predicted by movement time.

Adult↗

PubMed2006

Occlusal disharmony induces spatial memory impairment and hippocampal neuron degeneration via stress in SAMP8 mice.

We examined the effect of occlusal disharmony in senescence-accelerated (SAMP8) mice on plasma corticosterone levels, hippocampal neuron number, and spatial performance in the water maze. The bite-raised condition was associated with an accelerated age-related decline in spatial memory, increased plasma corticosterone levels, and a decreased number of neurons in the hippocampal CA3 region. The findings suggest that the bite-raised condition in aged SAMP8 mice induces hippocampal neuron loss, thereby leading to senile memory deficits.

Aging↗

PubMed1996

Spatial locations gone awry: object and spatial memory deficits in children with fetal alcohol syndrome.

Hippocampus vulnerability following gestational alcohol exposure has been demonstrated neuroanatomically and behaviorally in animal models of fetal alcohol syndrome (FAS). There has been no similar demonstrations in humans. The Smith and Milner (1981) Memory for 16 Objects task has been used to explore the effects of right vs left temporal lobectomy with varying degrees of damage to the hippocampus. In the present experiment, this same task was administered to 15 children with FAS (mean age 10.03, S.D. = 2.33) and 15 control children (mean age 10.02, S.D. = 2.31). Similar to patients with right temporal lobectomies and a large excision to the hippocampus, children with FAS were able to perform immediate but not delayed object recall, had a general spatial memory deficit (P < 0.05), and significantly distorted the spatial array (P < 0.05). Although these results are consistent with an interpretation of hippocampal dysfunction, gestational alcohol exposure is known to result in a wide-ranging spectrum of neuropsychological deficits that vary in both extent and severity. Visuospatial deficits on the Beery test of Visuomotor Integration and Clock Drawing are suggestive of the other neural regions that may be involved in producing the behavioral deficits in children with FAS.

Adolescent↗

PubMed2006

Hippocampal up-regulation of NCAM expression and polysialylation plays a key role on spatial memory.

Memory formation has been associated with structural and functional modifications of synapses. Cell adhesion molecules are prominent modulators of synaptic plasticity. Here, we investigated the involvement of the cell adhesion molecules, NCAM, its polysialylated state (PSA-NCAM) and L1 in spatial learning-induced synaptic remodeling and memory storage. A differential regulation of these adhesion molecules was found in the hippocampus of rats submitted to one training session in the spatial, but not cued, version of the Morris water maze. Twenty-four hours after training, synaptic expression of NCAM and PSA-NCAM was increased, whereas L1 appeared markedly decreased. The regulation of these molecules was spatial learning-specific, except for L1 reduction, which could be attributed to swimming under stressful conditions rather than to learning. Subsequent psychopharmacological experiments were performed to address the functional role of NCAM and PSA-NCAM in the formation of spatial memories. Rats received an intracerebroventricular injection of either a synthetic peptide (C3d) aimed to interfere with NCAM function, or endoneuraminidase, an enzyme that cleaves polysialic acid from NCAM. Both treatments affected acquisition of spatial information and lead to impaired spatial memory abilities, supporting a critical role of the observed learning-induced up-regulation of synaptic NCAM expression and polysialylation on spatial learning and memory. Therefore, our findings highlight NCAM as a learning-modulated molecule critically involved in the hippocampal remodeling processes underlying spatial memory formation.

Animals↗

PubMed2001

Normal spatial memory following postseizure treatment with ketamine: selective damage attenuates memory deficits in brain-damaged rodents.

Within 30 min after the initiation of status epilepticus (SE) by lithium and pilocarpine, rats were injected with either acepromazine or ketamine. Compared to the rats that had received the acepromazine, the group that had received the ketamine displayed more accurate spatial memory. Their scores did not differ significantly from normal (non-seized) controls. Although the ketamine treatment did not significantly change the amount of neuronal loss within about 100 Paxinos and Watson structures, it was neuroprotective for several structures within the thalamus and portions of the temporal and parietal cortices. Ketamine-treated rats, however, displayed markedly more damage within the entorhinal cortices and amygdalohippocampal area.

Acepromazine↗

PubMed2006

NF-kappaB regulates spatial memory formation and synaptic plasticity through protein kinase A/CREB signaling.

Synaptic activity-dependent de novo gene transcription is crucial for long-lasting neuronal plasticity and long-term memory. In a forebrain neuronal conditional NF-kappaB-deficient mouse model, we demonstrate here that the transcription factor NF-kappaB regulates spatial memory formation, synaptic transmission, and plasticity. Gene profiling experiments and analysis of regulatory regions identified the alpha catalytic subunit of protein kinase A (PKA), an essential memory regulator, as a new NF-kappaB target gene. Consequently, NF-kappaB inhibition led to a decrease in forskolin-induced CREB phosphorylation. Collectively, these results disclose a novel hierarchical transcriptional network involving NF-kappaB, PKA, and CREB that leads to concerted nuclear transduction of synaptic signals in neurons, accounting for the critical function of NF-kappaB in learning and memory.

Animals↗

PubMedDate not supplied

Retrieval induces hippocampal-dependent reconsolidation of spatial memory.

Nonreinforced retrieval can cause extinction and/or reconsolidation, two processes that affect subsequent retrieval in opposite ways. Using the Morris water maze task we show that, in the rat, repeated nonreinforced expression of spatial memory causes extinction, which is unaffected by inhibition of protein synthesis within the CA1 region of the dorsal hippocampus. However, if the number of nonreinforced retrieval trials is insufficient to induce long-lasting extinction, then a hippocampal protein synthesis-dependent reconsolidation process recovers the original memory. Inhibition of hippocampal protein synthesis after reversal learning sessions impairs retention of the reversed preference and blocks persistence of the original one, suggesting that reversal learning involves reconsolidation rather than extinction of the original memory. Our results suggest the existence of a hippocampal protein synthesis-dependent reconsolidation process that operates to recover or update retrieval-weakened memories from incomplete extinction.

Animals↗

PubMed2003

Testing the importance of the caudal retrosplenial cortex for spatial memory in rats.

Although there is evidence to suggest that the retrosplenial cortex is involved in spatial learning and memory, many lesion studies have left the more caudal part of this region intact so leaving its role untested. In the first experiment, rats with neurotoxic lesions of the caudal half of the retrosplenial cortex (RspC1) were tested on a reference memory task in the water-maze. The RspC1 animals were impaired on initial acquisition although they performed normally on a subsequent probe test. The second experiment looked at working memory in the radial-arm maze and water-maze. Animals with caudal retrosplenial lesions (RspC2) were unimpaired on the acquisition stage of the radial-arm maze task but were impaired when the task involved maze rotation to control for the possible use of intramaze cues. The RspC2 animals also took longer to learn the platform position on a delayed matching-to-place task in the water-maze. These results show a subtle impairment in spatial memory performance that is not as severe as that seen when more complete lesions of the retrosplenial cortex are made.

Animals↗

PubMed2005

Prenatal zinc treatment at the time of acute ethanol exposure limits spatial memory impairments in mouse offspring.

Zinc (Zn) treatment given together with acute ethanol in early pregnancy has previously been demonstrated to protect against physical birth abnormalities in mice. The current study examined whether this Zn treatment (s.c. injection) can also prevent the more subtle cognitive impairments caused by ethanol exposure in early pregnancy. Pregnant C57BL/6J dams were injected with saline (0.85% wt/vol NaCl) or 25% ethanol (0.015 mL/g body weight) intraperitoneally at 0 and 4 h on gestational d (GD) 8. ZnSO4 (2.5 microg Zn/g at 0 h) treatment was administered by s.c. injection immediately following ethanol treatment. Offspring were randomly selected from litters for each of the three treatment groups and were tested at 55 and 70 d of age using a cross-maze water escape task for spatial learning and memory impairments consecutively. No differences were observed between treatments for the spatial learning task. However, young adult mice exposed to ethanol in utero demonstrated impaired spatial memory, with a decrease in correct trials and increased escape latency and incorrect entry measurements, compared with saline-treated controls. In comparison, offspring given s.c. Zn treatment at the time of ethanol exposure were not cognitively impaired, performing at the same level as control mice in the cross-maze escape task. These findings indicate that critically timed Zn administration can limit spatial memory impairments caused by ethanol exposure in early pregnancy.

Animals↗

PubMed2006

Spatial memory activation of the parietal cortex measured with near-infrared spectroscopic imaging in the finger-maze of the Morris water maze analogue for humans.

To assess the cortical regions involved in learning spatial navigation, changes in oxyhemoglobin volume were measured with near-infrared spectroscopy in a task analogous to the Morris water maze. The blindfolded participants (Ps) were allowed to search the area inside the circular ring (20 cm) until they reached a goal (1 cm). The sitting and starting positions were randomly varied across trials, but the goal was in a fixed position so that the Ps could learn the allocentric spatial relationship between the goal and the experimental room. There was a significant sex difference (p < 0.05) in the present task, showing that performance in males was better than that in females. With this task, we measured brain activation in the first training trial, the probe test, and the motor-control trials. In the first trial, dorsolateral prefrontal and parietal cortices were activated. In the probe test, only the dorsolateral prefrontal regions were activated. These results suggest that the parietal cortex is critical for acquisition of spatial memory.

Adult↗

PubMed2006

Impaired spatial memory in APP-overexpressing mice on a homocysteinemia-inducing diet.

Consumption of a diet that significantly elevates homocysteine (homocysteinemia) induces cell death in the CA3 hippocampal subfield in amyloid precursor protein (APP) over-expressing transgenic mice but not in wild-type controls. We assessed behavioral and other neuropathological effects of a homocysteinemia-inducing diet in aged APP-overexpressing mice. Starting at 16-18 months of age, mice were fed either a treatment diet lacking folate, choline, and methionine, and supplemented with homocysteine, or a control diet containing normal amounts of folate, choline and methionine but no homocysteine. After 5 months on the experimental diets, performance on a delayed non-matching-to-position working-memory task was unimpaired. In contrast, spatial reference memory in the water maze was impaired in transgenic mice on the treatment diet. Transgenic mice had higher homocysteine levels than wild-type mice even when fed the control diet, suggesting an effect of genotype on homocysteine metabolism. Methyl-donor deficiency did not alter amyloid deposition in the transgenic mice. These results suggest that disrupted homocysteine metabolism may induce Abeta-associated memory impairments and neurodegeneration in APP overexpressing mice.

Amyloid beta-Protein Precursor↗

PubMed1994

Effects of adrenalectomy on spatial memory performance and dentate gyrus morphology.

Adrenalectomy (ADX) causes neuronal degeneration and cell loss in the dentate gyrus (DG) of the hippocampus. Since chemical or mechanical lesions of the DG are associated with impairments of spatial memory in rats, the effects of ADX on radial arm maze performance were evaluated. During 15 trials, where all 8 arms of the maze were baited, ADX rats were significantly impaired compared to sham operated controls (Shams). These trials were conducted 21-42 days post-ADX. Following these trials, time delays were instituted between the 4th and 5th choices, and ADX rats continued to show impaired performance. Daily intake of 3% saline was monitored in all rats and serum corticosterone (Cort) was measured. Saline consumption (ml/day) was higher in the ADX group (16.9 +/- 1.6 in ADX vs. 1.3 +/- 0.3 in Shams) and was negatively correlated with Cort level. Serum Cort (% microgram) differed between groups (0.6 +/- 0.4 vs. 15.0 +/- 2.3) and was negatively correlated with a greater number of maze errors, a measure of impaired performance. Cross sectional DG area was not reduced in ADX rats, and pyknotic cell number did not differ significantly between ADX and Sham animals. Moreover, pyknotic cell counts did not correlate with behavioral measures. These results lead to two conclusions: First, the recovery of accessory adrenal tissue in ADX rats, as indicated by the low levels of Cort, appears sufficient to suppress dentate granule neuron pyknosis, but may not be sufficient to suppress salt appetite.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗