Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Spatial memory”

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 1,657 records · Page 92Linked to original sources

The separability of working memory resources for spatial thinking and language processing: an individual differences approach.

The current study demonstrates the separability of spatial and verbal working memory resources among college students. In Experiment 1, we developed a spatial span task that taxes both the processing and storage components of spatial working memory. This measure correlates with spatial ability (spatial visualization) measures, but not with verbal ability measures. In contrast, the reading span test, a common test of verbal working memory, correlates with verbal ability measures, but not with spatial ability measures. Experiment 2, which uses an interference paradigm to cross the processing and storage demands of span tasks, replicates this dissociation and further demonstrates that both the processing and storage components of working memory tasks are important for predicting performance on spatial thinking and language processing tasks.

Adult↗

Protective effects of inosine on mice subjected to lethal total-body ionizing irradiation.

Mammals can barely survive total-body ionizing irradiation greater than 10 Gy. To date, there are few drugs available for radioprotective therapy under such circumstances. Inosine, a natural derivative of adenosine, has been known to provide powerful protection for many kinds of cells and tissues against various insults both in vitro and in vivo. In the present study, we examined whether inosine was also beneficial for mammals subjected to an absolutely lethal total-body ionizing irradiation. Immediately after adult Balb/c mice were exposed to (60)Co gamma-rays at a single dose of 12 Gy, a moiety of them were administered daily with inosine or adenosine, either at doses of 375 or 750 micromol/kg up to death, and their body weight and survival time were recorded. Some irradiated mice were administered inosine or adenosine daily at doses of 750 micromol/kg and assessed for spatial memory abilities using the Morris water maze. The results demonstrated that, although inosine could not prevent body weight loss in irradiated mice, it was able to significantly prolong their survival time at doses of 750 micromol/kg. Moreover, inosine but not adenosine could suppress spatial memory deficit in irradiated mice. The data suggested that inosine had protective effects on mammals suffering from total-body ionizing irradiation at a single lethal dose.

Animals↗

The 17alpha and 17beta isomers of estradiol both induce rapid spine synapse formation in the CA1 hippocampal subfield of ovariectomized female rats.

Previous studies have demonstrated that estradiol-17beta and estradiol-17alpha both induce short-latency effects on spatial memory in rats, estradiol-17alpha being at least as potent as its 17beta isomer. To determine whether the mechanisms underlying these behavioral responses might include effects on hippocampal synaptic plasticity, CA1 pyramidal spine synapse density (PSSD) was measured in ovariectomized rats within the first few hours after s.c. estrogen injection. PSSD increased markedly (by 24%) 4.5 h after the administration of 45 microg/kg estradiol-17beta. The PSSD response was significantly greater (44% above control) 30 min after estradiol-17beta injection and was markedly dose dependent; a 3-fold lower estradiol-17beta dose (15 microg/kg) did not significantly affect CA1 PSSD at either 30 min or 4.5 h. Estradiol-17alpha was a more potent inducer of PSSD than estradiol-17beta. Dose-response analysis determined an ED50 for the effect of estradiol-17alpha on PSSD of 8.92 +/- 1.99 microg/kg, with a maximal response at 15 microg/kg. These results demonstrate that high doses of estradiol induce rapid changes in CA1 PSSD. CA1 spine synapse formation appears to be more sensitive to estradiol-17alpha than to estradiol-17beta, paralleling previous data on the effects of these two steroids on spatial memory. Rapid remodeling of hippocampal synaptic connections may thus contribute to the enhancement of spatial mnemonic processing observed within the first few hours after estrogen treatment. The potency of estradiol-17alpha suggests that hormone replacement therapy using this steroid might be useful clinically in ameliorating the impact of low endogenous estrogen production on the development and progression of neurodegenerative disorders involving the hippocampus.

Animals↗

ERbeta-selective SERMs produce mnemonic-enhancing effects in the inhibitory avoidance and water maze tasks.

Estradiol (17beta-E2) can have mnemonic-enhancing effects; however, its mechanisms for these effects are not well-understood. The present studies examined effects of 17beta-E2 and selective estrogen receptor modulators (SERMs) on emotional and spatial memory of female, Long-Evans rats. First, whether or not 17beta-E2 has dose-dependent effects on inhibitory avoidance memory was investigated. Only the highest concentration of 17beta-E2 examined (10 microg), which produces physiological concentrations of E2, was effective at enhancing inhibitory avoidance memory (Experiment 1). Further studies were designed to elucidate whether SERMs may produce mnemonic effects similar to those of 17beta-E2. Compounds utilized were, the ERalpha-selective SERMs, propyl pyrazole triol (PPT) or 17alpha-E2, the ERbeta-specific SERMs, diarylpropionitrile (DPN) or 7,12-dihydrocoumestan (coumestrol), or vehicle (oil). Post-training administration of 10 microg 17beta-E2 or coumestrol enhanced memory in the inhibitory avoidance task compared to vehicle (Experiment 2). Memory in the water maze was enhanced by post-training administration of 17beta-E2, coumestrol, or DPN, compared to vehicle (Experiment 3). Co-administration of 17alpha-E2&DPN enhanced inhibitory avoidance memory similar to that seen following 17beta-E2 or coumestrol (Experiment 4). Administration of E2 2 h post-training was not effective at enhancing memory in the inhibitory avoidance or water maze tasks (Experiment 5). Lordosis of rats was enhanced by 17beta-E2, 17alpha-E2, or PPT, compared to vehicle (Experiment 6). These data suggest that: E2's actions at ERbeta, rather than ERalpha, may enhance spatial memory, E2's actions at ERalpha can facilitate sexual behavior, and that E2's actions involving both ERalpha and ERbeta may be important for emotional memory.

Animals↗

A behavioral and histological study of the effects of long-term exposure of adult rats to aluminum.

Aluminum (Al) has been etiologically and epidemiologically related to several neurologic conditions, including Alzheimer's disease (AD). The effects of Al long-term exposure were investigated to describe the associated behavioral and brain modifications. Adult rats were intraperitoneally injected three times a week for 6 months with ecological doses of Al gluconate (0.85 mg/kg). The Al overload was confirmed by the significantly increased level of Al in serum. We assessed fear conditioning, spatial memory and emotional reactivity by shuttle-box task, Morris water maze, and open-field, respectively. The performance of the experimental animals at the shuttle-box task was significantly lower (p <.01) compared to that of control. The experimental animals had impaired spatial memory, with lower and more fluctuant performance at Morris water maze. The noxious-driven behavior of the experimental animals was also altered, with significantly lower activity scores (p <.05), and high emotionality scores (p <.01) at the open-field. We recovered and processed the brain for aluminum and amyloid deposits. The brains of experimental animals, studied by optical microscopy, displayed a massive cellular depletion in the hippocampal formation, particularly, the CAl field, and also in the temporal and parietal cortex. We observed numerous ghost-like neurons with cytoplasmic and nuclear vacuolations, and with Al deposits. The hippocampus contained extracellular accumulations of Al and amyloid surrounded by nuclei of degenerating cells, which we interpreted as neuritic plaques. The cerebrovasculature was distorted, with a significant thickening of the wall of capillaries, associated with amyloid deposits. These behavioral and neuropathological modifications associated with long-term exposure to Al are reminiscent of those observed in AD.

Aluminum↗

Effects of pyrrolidine dithiocarbamate on beta-amyloid (25-35)-induced inflammatory responses and memory deficits in the rat.

It has been well established that neuroinflammation is involved in Alzheimer disease (AD) pathogenesis. Accumulation and aggregation of beta-amyloid (Abeta) peptide in the brains of patients with AD result in activation of glial cells which, in turn, initiates neuroinflammatory responses that involve reactive oxygen intermediates and release of inflammatory cytokines. In this study, bilateral intracerebroventricular (i.c.v.) injections of Abeta (25-35) in the rat resulted in impairment in learning and spatial memory and increased immunoreactive staining of AD-related neuropathological markers (Abeta, APP) and inflammatory mediators (OX-6, COX-2) in CA1 and dentate gyrus regions of the hippocampus. Pyrrolidine dithiocarbamate (PDTC) given intraperitoneally 30 min before Abeta injection and daily for 7 days postsurgery significantly prevented Abeta-induced neuropathological and neuroinflammatory responses, as well as the learning and spatial memory deficits. The potential of PDTC for reducing cognitive and neuropathological deficits may provide preliminary evidence for a new approach of AD treatment.

Amyloid beta-Peptides↗

Pharmacological antagonism of metabotropic glutamate receptor 1 regulates long-term potentiation and spatial reference memory in the dentate gyrus of freely moving rats via N-methyl-D-aspartate and metabotropic glutamate receptor-dependent mechanisms.

Group I metabotropic glutamate receptors (mGluRs) are critically required for multiple forms of hippocampal synaptic plasticity in vivo. The role of the receptor subtype mGluR1 in long-term potentiation (LTP) and learning is unclear. We examined the contribution of mGluR1 to hippocampal LTP and spatial learning using the selective antagonist (S)-(+)-alpha-amino-4carboxy-2-methylbenzene-acetic acid (LY367385). Male Wistar rats were chronically implanted with recording and stimulating electrodes to enable measurement of evoked potentials from medial perforant path-dentate gyrus granule cell synapses. An injection cannula was inserted into the ipsilateral cerebral ventricle to enable drug application. Experiments were begun 10 days after the implantation procedure. We induced a robust LTP which lasted over 25 h with a 200-Hz tetanization. Injections of LY367385 at all concentrations under investigation (4-32 nmol in a 5-microL injection volume) did not affect basal synaptic transmission. In contrast, we observed a dose-dependent impairment of LTP expression: LY367385 (4 nmol) had no effect on LTP induction, whereas 8 and 16 nmol LY367385 reduced both LTP induction and expression, suggestive of an interaction with N-methyl-d-aspartate receptors. We assessed the effects of daily LY367385 application (8 nmol) on performance in an eight-arm radial maze. LY367385-treated rats showed deficits in reference but not working memory performance compared with vehicle-treated controls. Rearing, grooming and locomotor activity were unaffected by LY367385. These data suggest an important role for mGluR1 in LTP and learning and highlight the specific significance of this mGluR subtype for reference memory.

Analysis of Variance↗

Mechanisms of amnestic effect of ergot alkaloid agroclavin.

Neurochemical mechanisms of the effect of agroclavin on spatial memory in the Morris water maze in mice were studied by analyzing the effect of neurotransmitter receptor ligands on the amnestic effect of this alkaloid. D1-receptor agonist SKF-38393 and calcium channel blockers verapamil and nimodipine abolished the negative effect of agroclavin on spatial memory. The role of intracellular calcium in the mechanisms of amnestic effect of agroclavin is discussed.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Parallel instabilities of long-term potentiation, place cells, and learning caused by decreased protein kinase A activity.

To further elucidate the links among synaptic plasticity, hippocampal place cells, and spatial memory, place cells were recorded from wild-type mice and transgenic "R(AB)" mice with reduced forebrain protein kinase A (PKA) activity after introduction into a novel environment. Place cells in both strains were similar during the first exposure and were equally stable for recording sessions separated by 1 hr. Place cell stability in wild-type mice was unchanged for sessions separated by 24 hr but was reduced in R(AB) mice over the longer interval. This stability pattern parallels both the reduced late-phase long-term potentiation in hippocampal slices from R(AB) mice and the amnesia for context fear conditioning seen in R(AB) mice 24 but not 1 hr after training. The similar time courses of synaptic, network, and behavioral instability suggest that the genetic reduction of PKA activity is responsible for the defects at each level and support the idea that hippocampal synaptic plasticity is important in spatial memory.

Action Potentials↗

Effect of batroxobin on expression of neural cell adhesion molecule in temporal infarction rats and spatial learning and memory disorder.

The effect of Batroxobin expression of neural cell adhesion molecule (NCAM) in left temporal ischemic rats with spatial memory disorder was investigated by means of Morri's water maze and immunohistochemical methods. The results showed that the mean reaction time and distance of temporal ischemic rats for searching a goal were significantly longer than those of sham-operated rats and at the same time NCAM expression of left temporal ischemic region was significantly increased. However, the mean reaction time and distance of Batroxobin-treated rats were shorter and they used normal strategies more often and earlier than those of ischemic rats. The number of NCAM immune reactive cells of Batroxobin-treated rats was more than that of ischemic group. In conclusion, Batroxobin can improve spatial memory disorder of temporal ischemic rats and the regulation of the expression of NCAM is probably related to the neuroprotective mechanism.

Animals↗

Neuroprotective effects of novel cholinesterase inhibitors derived from rasagiline as potential anti-Alzheimer drugs.

TV3326, (N-propargyl-(3R)-aminoindan-5-yl-ethyl,methyl carbamate) was prepared in order to combine the neuroprotective effects of rasagiline, a selective inhibitor of monoamine oxidase (MAO)-B with the cholinesterase (ChE) inhibitory activity of rivastigmine as a potential treatment for Alzheimer's disease. The study reported here examined the neuroprotective effects of TV3326 against various insults in vitro and in vivo. TV3326 caused a dose related (10-500 microM) reduction in death induced in NGF differentiated rat pheochromocytoma (PC12) cells by 3-4 hour exposure to oxygen-glucose deprivation. A single s.c. injection of TV3326 given five minutes after closed head injury in mice significantly reduced the cerebral edema, and accelerated the recovery of motor function and spatial memory several days later. Unilateral icv injection of streptozotocin (STZ) 1.5 mg in rats, caused specific damage to myelinated neurones in the fornix and corpus callosum accompanied by microgliosis. Three bilateral injections of STZ, 0.25 mg each, caused more widespread damage, and a marked impairment in spatial memory. Chronic oral treatment with TV3326 (75 mumols/kg) reduced the neuronal damage and microgliosis and almost completely prevented the memory impairment. The neuroprotective effect in PC12 cells may be due to a combination of ChE inhibition and antiapoptotic activity. The latter does not result from ChE inhibition. It is associated with the presence of the propargyl group, since it occurs with other propargylamines that do not inhibit MAO, but not with drugs that inhibit only ChE.

Alzheimer Disease↗

Centrophenoxine improves chronic cerebral ischemia induced cognitive deficit and neuronal degeneration in rats.

AIM: To study the effects of centrophenoxine (CPH, meclofenoxate) on chronic cerebral hypoperfusion induced deficits in rats. METHODS: Chronic hypoperfusion in rats was performed by permanent bilateral ligation of the common carotid arteries. Morris water maze was used to measure spatial memory performance. Spectrophotometrical techniques were used to assay SOD, GPx activities, MDA content, TXB2, and 6-keto-PGF1alpha levels. Morphological change was examined by HE staining. The expression of Bax and p53 protein were assayed by immunohistochemistry analysis. RESULTS: Chronic hypoperfusion in rats resulted in spatial memory impairments shown by longer escape latency and shorter time spent in the target quadrant. These behavioral dysfunction were accompanied by increase in SOD and GPx activities, the content of MDA, the levels of pro-inflammatory mediators (TXB2, 6-keto-PGF1alpha), overexpression of Bax and P53 protein, and delayed degeneration of neurons in cortex and hippocampus. Oral administration of CPH (100 mg/kg, once per day for 37 d) markedly improved the memory impairment, reduced the increase in antioxidant enzyme activities, MDA content and the levels of pro-inflammatory mediators to their normal levels, and attenuated neuronal damage. CONCLUSION: The abilities of CPH to attenuate memory deficits and neuronal damage after ischemia may be beneficial in cerebrovascular type dementia.

Animals↗

Rap1 couples cAMP signaling to a distinct pool of p42/44MAPK regulating excitability, synaptic plasticity, learning, and memory.

Learning-induced synaptic plasticity commonly involves the interaction between cAMP and p42/44MAPK. To investigate the role of Rap1 as a potential signaling molecule coupling cAMP and p42/44MAPK, we expressed an interfering Rap1 mutant (iRap1) in the mouse forebrain. This expression selectively decreased basal phosphorylation of a membrane-associated pool of p42/44MAPK, impaired cAMP-dependent LTP in the hippocampal Schaffer collateral pathway induced by either forskolin or theta frequency stimulation, decreased complex spike firing, and reduced the p42/44MAPK-mediated phosphorylation of the A-type potassium channel Kv4.2. These changes correlated with impaired spatial memory and context discrimination. These results indicate that Rap1 couples cAMP signaling to a selective membrane-associated pool of p42/44MAPK to control excitability of pyramidal cells, the early and late phases of LTP, and the storage of spatial memory.

Animals↗

The role of body-based sensory information in the acquisition of enduring spatial representations.

Although many previous studies have shown that body-based sensory modalities such as vestibular, kinesthetic, and efferent information are useful for acquiring spatial information about one's immediate environment, relatively little work has examined how these modalities affect the acquisition of long-term spatial memory. Three groups of participants learned locations along a 146 m indoor route, and subsequently pointed to these locations, estimated distances between them, and constructed maps of the environment. One group had access to visual, proprioceptive, and inertial information, another had access to matched visual and matched inertial information, and another had access only to matched visual information. In contrast to previous findings examining transient, online spatial representations, our results showed very few differences among groups in the accuracy of the spatial memories acquired. The only difference was the improved pointing accuracy of participants who had access to proprioceptive information relative to that of participants in the other conditions. Results are discussed in terms of differential sensory contributions to transient and enduring spatial representations.

Adult↗

Longitudinal evaluation of memory performance and peripheral neuropathy in the Ins2C96Y Akita mice.

Ins2C96Y Akita mice represent a model of spontaneous early-onset diabetes mellitus, expressing a mutant non-functional isoform of insulin. These mice are characterized by a reduced number of pancreatic beta cells resulting in hypoinsulinemia and hyperglycemia. We obtained longitudinal measures of morning fasting blood glucose levels and gait performance. Sciatic nerve electrophysiology was also performed and the performance of these mice on spatial memory tasks was measured longitudinally. We observed a progressive increase in fasting blood glucose levels that was proportionally associated with increased gait disturbances. Diabetes induced a decrease in the sensory nerve conduction velocity up to the age of 40 weeks. Glucose transporter (GLUT) 3 levels were reduced in the hippocampus of the aged Ins2C96Y Akita mice. However, we failed to detect any significant deficits during reference, reversal or probe tests in the Morris water maze or in a spontaneous alternation task up to the age of 34 weeks old. We found that, up to the age of 34 weeks old, uncontrolled hyperglycemia produced peripheral neuropathy and reduced hippocampal GLUT3 levels in the absence of any effect on spatial memory processing.

Age Factors↗

How rats perform spatial working memory tasks: limitations in the use of egocentric and idiothetic working memory.

Rats of the Dark Agouti strain were trained on delayed alternation under conditions that should encourage egocentric working memory. In two experiments a T-maze was set within a cross-maze so that different arms could be used for the sample and test runs. The maze had high opaque side-walls, and testing was conducted in low light levels so that distal visual cues might be eliminated. By rotating the maze 90 degrees between the sample and choice run and by using two identical mazes set side by side it was possible to nullify other spatial strategies. Experiments 1 and 2 showed that rats preferentially used place information, intramaze cues, and direction cues, even though only egocentric or idiothetic (nonmatch-to-turn) working memory could successfully solve every trial. Rats were able to maintain an accurate sense of location within the maze even though distal cues were not visible and the animal was moved between the sample and choice runs. Experiment 2 confirmed that another rat strain (Long-Evans) shows the same learning profiles. Both experiments indicate that rats are very poor at using either egocentric or idiothetic information to alternate, and that retention delays as short as 10 s can eliminate the use of these forms of memory.

Animals↗

Is hippocampal volume affected by specialization for food hoarding in birds?

The hypothesis that spatial-memory specialization affects the size of the hippocampus has become widely accepted among scientists. The hypothesis comes from studies on birds primarily in two families, the Paridae (tits, titmice and chickadees) and the Corvidae (crows, nutcrackers, jays, etc.). Many species in these families store food and rely on spatial memory to relocate the cached items. The hippocampus is a brain structure that is thought to be important for memory. Several studies report that hoarding species in these families possess larger hippocampi than non-hoarding relatives, and that species classified as large-scale hoarders have larger hippocampi than less specialized hoarders. We have investigated the largest dataset on hippocampus size and food-hoarding behaviour in these families so far but did not find a significant correlation between food-hoarding specialization and hippocampal volume. The occurrence of such an effect in earlier studies may depend on differences in the estimation of hippocampal volumes or difficulties in categorizing the degree of specialization for hoarding or both. To control for discrepancies in measurement methods we made our own estimates of hippocampal volumes in 16 individuals of four species that have been included in previous studies. Our estimates agreed closely with previous ones, suggesting that measurement methods are sufficiently consistent. Instead, the main reasons that previous studies have found an effect where we did not are difficulties in assessing the degree of hoarding specialization and the fact that smaller subsets of species were compared than in our study. Our results show that a correlation between food-hoarding specialization and hippocampal volume cannot be claimed on the basis of present data in these families.

Adaptation, Physiological↗

[Long-term effects of neonatal recurrent seizures on gamma-aminobutyric acid A receptor alpha1 and gamma2 subunit expressions in the rat brain].

OBJECTIVE: To investigate the long-term effects of flurothyl-induced neonatal recurrent seizures on GABA A receptor (GABA(A)R) alpha1 and gamma2 subunit expressions in adult rat brain, and discuss the relationship between these alterations of GABA(A)R subunits in mature brain and the changes of spatial memory and seizure susceptibility in adult rats. METHODS: Thirty-two of 7-day-old (P7) Sprague-Dawley rats were divided randomly into two groups: the control group and the seizure group. Seizures were induced by inhalant flurothyl daily for six consecutive days. Rats were tested for spatial memory by using the Morris water maze task from postnatal 61 d(P61) to P65. Seizure threshold was examined by intraperitoneal injection of pentylenetetrazol, and then the brains were sampled on P75. The expressions of GABA(A)R alpha1 and gamma2 subunits mRNA and protein in cerebral cortex and hippocampus were detected by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry method. RESULTS: On P64, the escape latencies in water maze for the rats in the seizure group were significantly longer than those of the control rats [(82 424+/-35 622)ms vs (40 712+/-29 468)ms, P=0.001]. On P65, the frequency of crossing target within 120 s in water maze for the rats in the seizure group were significantly less than those of the control rats [(1.2+/-0.9) vs (3.1+/-1.3), P<0.001]. There was no difference in seizure threshold between the two groups on P75 [(1 487+/-662)s vs (1 841+/-648)s, P=0.137]. Compared to the control rats, the accumulated optical density (AOD) of GABA(A)R alpha1 subunit immunoreactivity in seizure rats decreased significantly in the parietal cortex, CA1-2 and CA4 region (P<0.05). The AOD of alpha1 subunit protein immunoreactivity in the frontal cortex, CA3 and dentate gyrus (DG) were of no significant difference between the two groups on P75 (P>0.05). There were also no differences in the AOD of gamma2 subunit protein immunoreactivity in the parietal lobe, DG, and CA1-3 region between the two groups (P>0.05). The AOD of gamma2 subunit protein immunoreactivity in the frontal lobe and CA4 region decreased significantly in the seizure group than those in the control group (P<0.05). The expressions of alpha1 subunits mRNA in the cerebral cortex and gamma2 subunit mRNA in the hippocampus were similar between the two groups (P>0.05), but the expressions of alpha1 subunits mRNA in the hippocampus and gamma2 subunit mRNA in the cerebral cortex in the seizure group decreased significantly as compared with those in the control group (P< 0.05). CONCLUSION: Recurrent seizures in neonatal rats modify GABA(A) receptor alpha1 and gamma2 subunits expression in the cerebral cortex and hippocampus of adult rats, and cause long-term cognitive deficit, Which suggests that abnormal GABA(A) receptor expression might play an important role in long-term cognitive deficit induced by early life recurrent seizures.

Animals↗