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 1,153 records · Page 64Linked to original sources
PubMed1996

Involvement of entorhinal cortex or parietal cortex in long-term spatial discrimination memory in rats: retrograde amnesia.

Twenty-four rats assigned to 1 of 3 matched groups (control, entorhinal cortex [EC], and parietal cortex [PC]) were trained on 6 successive discrimination problems (2 in an 8-arm for pretraining and 4 in a 12-arm radial maze for training per se). The training on the 12-arm maze started 6, 4, 2, and 0.5 weeks before surgery. On the day after the rats learned the last problem, they were given surgery according to groups. Postoperative retention was measured by presenting 16 trials per session for each of the problems during 4 sessions. Results indicate that the EC lesions produced a retention deficit for problems learned immediately and up to 4 weeks before surgery, but not for the problem acquired 6 weeks before the lesions. The PC lesions produced a significant retrograde amnesia that was not temporally graded. Results demonstrate that the EC and PC make important, albeit distinct, contributions to spatial memory storage and retrieval in rats.

Amnesia, Retrograde↗
PubMed2004

Effects of cholinergic enhancement on visual stimulation, spatial attention, and spatial working memory.

We compared behavioral and neural effects of cholinergic enhancement between spatial attention, spatial working memory (WM), and visual control tasks, using fMRI and the anticholinesterase physostigmine. Physostigmine speeded responses nonselectively but increased accuracy selectively for attention. Physostigmine also decreased activations to visual stimulation across all tasks within primary visual cortex, increased extrastriate occipital cortex activation selectively during maintained attention and WM encoding, and decreased parietal activation selectively during maintained attention. Finally, lateralization of occipital activation as a function of the visual hemifield toward which attention or memory was directed was decreased under physostigmine. In the case of attention, this effect correlated strongly with a decrease in a behavioral measure of selective spatial processing. Our results suggest that, while cholinergic enhancement facilitates visual attention by increasing activity in extrastriate cortex generally, it accomplishes this in a manner that reduces expectation-driven selective biasing of extrastriate cortex.

Acetylcholine↗
PubMed1997

Spatial and non-spatial working memory at different stages of Parkinson's disease.

Groups of patients with Parkinson's disease, either medicated or unmedicated, were compared with a matched group of normal control subjects on a computerized battery of tests designed to assess spatial, verbal and visual working memory. In the spatial working memory task, subjects were required to search systematically through a number of boxes to find 'tokens' whilst avoiding those boxes in which tokens had previously been found. In the visual and verbal conditions, the subjects were required to search in exactly the same manner, but through a number of abstract designs or surnames, respectively, avoiding designs or names in which a token had previously been found. Medicated Parkinson's disease patients with severe clinical symptoms were impaired on all three tests of working memory. In contrast, medicated patients with mild clinical symptoms were impaired on the test of spatial working memory, but not on the verbal or visual working memory tasks. Non-medicated patients with mild clinical symptoms were unimpaired on all three tasks. These data are compared with the results of a previous study comparing groups of neurosurgical patients with frontal, temporal or amygdalo-hippocampectomy excisions on the same three tests of working memory. Taken together, the findings suggest that working memory deficits in Parkinson's disease emerge, and subsequently progress, according to a defined sequence, the evolution of which may be linked to the likely spatiotemporal progression of dopamine depletion within the striatum, in relation to the terminal distribution of its cortical afferents.

Antiparkinson Agents↗
PubMed2003

Sex differences in spatial and non-spatial Y-maze performance after chronic stress.

Chronic restraint is known to alter hippocampal CA3 dendritic morphology and spatial memory in male rats. The present study examined whether female rats, which exhibit different anatomical adaptations to chronic stress than those of males, would also show spatial memory impairments. Male and female Sprague-Dawley rats were restrained for 6 h/day for 21 days, a time frame previously demonstrated to cause hippocampal CA3 dendritic atrophy. The day after the last restraint session, rats were tested on a Y-maze, a habituation task that can be used to assess spatial memory. Chronic stress impaired Y-maze performance in both sexes without affecting levels of locomotion as measured by total arm entries in the first minute. However, Y-maze performance of stressed females improved in 2-5 min when chronically stressed males continued to show poor Y-maze performance. The enhanced Y-maze performance of chronically stressed females occurred when total arm entries were higher compared to the entries made by males. Therefore, correlations were performed between total arm entries and spatial memory in 1 and 2-5 min. In the first minute when control females demonstrated functional spatial memory, female controls with the lowest locomotor levels exhibited the best performance. The correlations for stressed females were not significant, and neither were the correlations for any group in 2-5 min. Overall, these results show important sex differences in response to chronic stress with females exhibiting an ability to recover quickly from deficits in Y-maze performance.

Animals↗
PubMed2000

A 5-arm maze enables parallel measures of sustained visuo-spatial attention and spatial working memory in mice.

A 5-arm maze has been developed to provide parallel tests of sustained visuo-spatial attention and spatial working memory in mice. C57Bl/6 mice were trained to select, either by immediate response (attention) or by delayed-matching response (working memory), one target arm among the five open arms. For attention testing, mice were first trained to acquire the basic task in which one randomly selected baited arm remained lit until a choice was made. Criterion of >80% correct with a response latency <5 s was attained in 52-56 trials. Following this, attention was tested by using trials wherein light signal durations of 2, 1 or 0.5 s were intermixed to vary attentional load. In the working memory test, mice were submitted to a forced visit to a randomly selected baited arm during a presentation phase. Following a variable retention interval (R.I.), mice were replaced into the maze and rewarded for choosing this arm. Criterion of >80% correct was attained in 35-40 trials and mice exhibited high levels of retention for R.I.s up to 4 h. Results validate the 5-arm maze for evaluation of both sustained visuo-spatial attention and spatial working memory in mice. Both the tasks are rapidly acquired and the 20% chance level provides high resolution for evaluating performance. This comparative strategy allows to dissociate attention and memory and to reveal deficits in these processes during ageing or in knockout strains. The high level of retention performance over R.I.s of 4 h enables studies using pharmacological treatments differentially affecting the acquisition, encoding, retention or retrieval phases of working memory. Furthermore, functional brain imaging studies may be used to identify neuronal networks which are differentially activated during these distinct phases.

Animals↗
PubMed2006

Development of a superior frontal-intraparietal network for visuo-spatial working memory.

Working memory capacity increases throughout childhood and adolescence, which is important for the development of a wide range of cognitive abilities, including complex reasoning. The spatial-span task, in which subjects retain information about the order and position of a number of objects, is a sensitive task to measure development of spatial working memory. This review considers results from previous neuroimaging studies investigating the neural correlates of this development. Older children and adolescents, with higher capacity, have been found to have higher brain activity in the intraparietal cortex and in the posterior part of the superior frontal sulcus, during the performance of working memory tasks. The structural maturation of white matter has been investigated by diffusion tensor magnetic resonance imaging (DTI). This has revealed several regions in the frontal lobes in which white matter maturation is correlated with the development of working memory. Among these is a superior fronto-parietal white matter region, located close to the grey matter regions that are implicated in the development of working memory. Furthermore, the degree of white matter maturation is positively correlated with the degree of cortical activation in the frontal and parietal regions. This suggests that during childhood and adolescence, there is development of networks related to specific cognitive functions, such as visuo-spatial working memory. These networks not only consist of cortical areas but also the white matter tracts connecting them. For visuo-spatial working memory, this network could consist of the superior frontal and intraparietal cortex.

Adolescent↗
PubMed2004

A relationship between cerebellar Purkinje cells and spatial working memory demonstrated in a lurcher/chimera mouse model system.

New emphasis has been placed upon cerebellar research because of recent reports demonstrating involvement of the cerebellum in non-motor cognitive behaviors. Included in the growing list of cognitive functions associated with cerebellar activation is working memory. In this study, we explore the potential role of the cerebellum in spatial working memory using a mouse model of Purkinje cell loss. Specifically, we make aggregation chimeras between heterozygous lurcher (Lc/+) mutant embryos and +/+ (wildtype) embryos and tested them in the delayed matching-to-position (DMTP) task. Lc/+ mice lose 100% of their Purkinje cells postnatally due to a cell-intrinsic gain-of-function mutation. Lc/+<->+/+ chimeras therefore have Purkinje cells ranging from 0 to normal numbers. Through histological examination of chimeric mice and observations of motor ability, we showed that ataxia is dependent upon both the number and distribution of Purkinje cells in the cerebellum. In addition, we found that Lc/+ mice, with a complete loss of Purkinje cells, have a generalized deficit in DMTP performance that is probably associated with their motor impairment. Finally, we found that Lc/+<->+/+ chimeric mice, as a group, did not differ from control mice in this task. Rather, surprisingly, analysis of their total Purkinje cells and performance in the DMTP task revealed a significant negative relationship between these two variables. Together, these findings indicate that the cerebellum plays a minor or indirect role in spatial working memory.

Animals↗
PubMed2001

Fluctuations in spatial recognition memory across the menstrual cycle in female rhesus monkeys.

Findings are inconsistent regarding whether women's cognitive performance fluctuates across phases of the menstrual cycle, but differences in methodology and the use of reported cycle phase rather than precise hormonal measures may underlie these disparities. Studies in monkeys may help resolve these discrepant findings, since hormonal status can be reliably determined. We tested four young (5-7 years old) female rhesus monkeys daily during one entire menstrual cycle on three cognitive tasks displayed on a computerized touch-screen system: a Matching to Sample task with a 30 s delay (MTS-30s), a Matching to Sample task without delay (MTS-no delay) and the spatial condition of the Delayed Recognition Span Test (spatial-DRST). Blood samples were collected at specific time intervals throughout the cycle and assayed for estradiol and progesterone in order to identify hormonal status. There was a nonsignificant trend for the MTS-30s scores to be better during the follicular and luteal phases, when estradiol levels were low, than during the peri-ovulatory phase, when estradiol levels were at their highest. MTS-no delay performance did not vary as a function of hormonal status. Spatial-DRST scores were significantly better during the follicular and luteal phases than during the peri-ovulatory phase of the cycle. These data in the female rhesus monkey support the hypothesis that spatial memory performance is sensitive to estradiol variations across the menstrual cycle, with better performance associated with low estradiol levels.

Animals↗
PubMed2003

Differential roles of dorsal hippocampal subregions in spatial working memory with short versus intermediate delay.

In order to determine the role of subregions of the hippocampus in spatial working memory, this study combined selective neurotoxic lesions of the hippocampal subregions with a simple delayed nonmatching-to-place task on a radial maze in rats. Lesions of the dentate gyrus or the CA3, but not the CA1, subregion of the hippocampus induced a deficit in the acquisition of the task with short-term delays (i.e., 10 sec) and impaired performance of the task in a novel environment. All subregional lesions produced sustained impairment in performing the task with intermediate-term delays (i.e., 5 min) when rats were tested in a familiar environment. The results suggest a dynamic interaction among the dorsal hippocampal subregions in processing spatial working memory, with the time window (i.e., delay) of a task recognized as an essential controlling factor.

Animals↗
PubMed2002

Attenuation of working memory and spatial acquisition deficits after a delayed and chronic bromocriptine treatment regimen in rats subjected to traumatic brain injury by controlled cortical impact.

Cognitive impairments are pervasive and persistent sequelae of human traumatic brain injury (TBI). In vivo models of TBI, such as the controlled cortical impact (CCI) and fluid percussion (FP), are utilized extensively to produce deficits reminiscent of those seen clinically with the hope that empirical study will lead to viable therapeutic interventions. Both CCI and FP produce spatial learning acquisition deficits, but only the latter has been reported to impair working memory in rats tested in the Morris water maze (MWM). We hypothesized that a CCI injury would impair working memory similarly to that produced by FP, and that delayed and chronic treatment with the D2 receptor agonist bromocriptine would attenuate both working memory and spatial learning acquisition deficits. To test these hypotheses, isoflurane-anesthetized adult male rats received either a CCI (2.7 mm deformation, 4 m/sec) or sham injury, and 24 h later were administered bromocriptine (5 mg/kg, i.p.) or vehicle, with continued daily injections until all behavioral assessments were completed. Motor function was assessed on beam balance and beam walking tasks on postoperative days 1-5 and cognitive function was evaluated in the MWM on days 11-15 for working memory (experiment 1) and on days 14-18 for spatial learning acquisition (experiment 2). Histological examination (hippocampal CA1 and CA3 cell loss/survival and cortical lesion volume) was conducted 4 weeks after surgery. All injured groups exhibited initial impairments in motor function, working memory, and spatial learning acquisition. Bromocriptine did not affect motor function, but did ameliorate working memory and significantly attenuated spatial acquisition deficits relative to the injured vehicle-treated controls. Additionally, the injured bromocriptine-treated group exhibited significantly more morphologically intact CA3 neurons than the injured vehicle-treated group (55.60 +/- 3.10% vs. 38.34 +/- 7.78% [p = 0.03]). No significant differences were observed among TBI groups in CA1 cell survival (bromocriptine, 40.26 +/- 4.74% vs. vehicle, 29.13 +/- 6.63% [p = 0.14]) or cortical lesion volume (bromocriptine, 17.78 +/- 0.62 mm3 vs. vehicle, 19.01 +/- 1.49 mm3 [p > 0.05]). These data reveal that CCI produces working memory deficits in rats that are similar to those observed following FP, and that the delayed and chronic bromocriptine treatment regimen conferred cognitive and neural protection after TBI.

Animals↗
PubMed2005

Abnormal expression of epilepsy-related gene ERG1/NSF in the spontaneous recurrent seizure rats with spatial learning memory deficits induced by kainic acid.

Previous epilepsy-related gene screen identified a spontaneous recurrent seizure (SRS)-related gene named epilepsy-related gene (ERG1) that encodes N-ethylmaleimide-sensitive fusion protein (NSF). To explore whether spatial learning memory deficits are relevant to SRS and whether hippocampal NSF expression is altered by SRS, we used the kainic acid (KA)-induced epilepsy animal model. SRS was monitored for 3 weeks after injection of a single convulsive dose of KA. KA-treated rats with SRS, KA-treated rats without SRS, and saline-treated rats were then measured in Morris water maze. In this spatial learning task, KA-treated rats with SRS performed poorer compared to those without SRS and those treated with saline. During the subsequent probe trials, KA-treated rats with SRS spent less swim path and time in the target quadrant but more swim path and time in the opposite quadrant, and showed fewer platform crossings. Moreover, in situ hybridization and immunohistochemistry showed that both ERG1/NSF mRNA and NSF immunoreactive expression were down-regulated in the CA1 and dorsal dentate gyrus cells (dDGCs) of the hippocampus, and interestingly, tyrosine hydroxylase (TH) immunoreactive dopamine (DA) neurons were lost in ventral tegmental area (VTA) in the KA rats with SRS. These data demonstrate that SRS impairs spatial learning memory and suggest that the down-regulation of NSF expression pattern in the hippocampus and the loss of DA neurons in VTA might contribute to the spatial learning memory deficits induced by SRS.

Animals↗
PubMed2004

Population vector analysis of primate prefrontal activity during spatial working memory.

Population vectors were used to examine information represented by a population of prefrontal activity and its temporal change during spatial working memory processes while monkeys performed ODR and R-ODR tasks. In the ODR task, monkeys made a saccade to the cue location after the delay, whereas in the R-ODR task, they made a saccade 90 degrees clockwise from the cue location. We first constructed population vectors using cue- and response-period activity. The directions of population vectors were similar to the cue directions and the saccade target directions, respectively, indicating that population vectors correctly represented information regarding directions of visual cues and saccade targets. We then calculated population vectors during a 250 ms time-window from the cue presentation to the end of the response period. In the ODR task, all population vectors were directed toward the cue direction. However, in the R-ODR task, the population vector gradually rotated during the delay period from the cue direction to the saccade direction. These results indicate that spatial information represented by a population of prefrontal activity can be shown as the direction of the population vector and that its temporal change during spatial working memory tasks can be depicted as the temporal change of the vector's direction.

Animals↗
PubMedDate not supplied

Extensive lesions of cholinergic basal forebrain neurons do not impair spatial working memory.

A recent study suggests that lesions to all major areas of the cholinergic basal forebrain in the rat (medial septum, horizontal limb of the diagonal band of Broca, and nucleus basalis magnocellularis) impair a spatial working memory task. However, this experiment used a surgical technique that may have damaged cerebellar Purkinje cells. The present study tested rats with highly selective lesions of cholinergic neurons in all major areas of the basal forebrain on a spatial working memory task in the radial arm maze. In postoperative testing, there were no significant differences between lesion and control groups in working memory, even with a delay period of 8 h, with the exception of a transient impairment during the first 2 d of postoperative testing at shorter delays (0 or 2 h). This finding corroborates other results that indicate that the cholinergic basal forebrain does not play a significant role in spatial working memory. Furthermore, it underscores the presence of intact memory functions after cholinergic basal forebrain damage, despite attentional impairments that follow these lesions, demonstrated in other task paradigms.

Acetylcholine↗
PubMed1997

Verbal and spatial working memory in school-age children: developmental differences in susceptibility to interference.

The development of verbal and spatial working memory was investigated with an interference paradigm. Memory spans were obtained from 3 groups (8-, 10-, and 19-year-olds) under 6 different conditions: Two primary memory tasks (1 verbal, 1 spatial) were administered in isolation and in conjunction with 2 versions of a secondary task. The primary tasks required recalling a series of visually presented digits and recalling the locations of Xs in a series of visually presented grids. The secondary tasks required reporting the color of the stimuli as they were presented using either a verbal or a spatial response. Analyses revealed that all age groups showed domain-specific interference (i.e., interference by a secondary task from the same domain as the primary task), but only the 8-year-olds also showed nonspecific interference (i.e., interference by a secondary task from a domain different than the primary memory task), suggesting that at least some executive functions do not reach adult levels of efficiency until approximately age 10.

Adolescent↗
PubMed1989

The effect of embryonal amygdala grafts on the impairment of spatial working memory elicited in rats by kainate-induced amygdaloid damage.

The effect of epileptogenic lesion of amygdala on spatial working memory was examined in rats after unilateral (U, n = 9) or bilateral (B, n = 8) injection of 1 or 0.5 mu of 0.2% kainate into the amygdaloid complex. Another group of unilaterally lesioned rats (T, n = 9) received 8 days after kainate injection grafts of embryonal (E 20) amygdala into the damaged region. Twelve days after lesion the three experimental groups and an unoperated control group (C, n = 11) were trained during three weeks in the aversively motivated 8-arm radial water maze (RWM). Training decreased incidence of errors/8 choices from the initial 2.3 to 1.2 in the lesioned rats and to 0.4 in the controls. Transplantation did not enhance RWM acquisition but restored the symmetrical pattern of choices and normalized the emotionality of lesioned animals. Retraining the RWM task 3 months later revealed significant savings in the control group but not in the transplanted group. Histology showed in addition to large lesion at the injection site also distant lesions in the ipsilateral hippocampus, thalamus and neocortex and in the unilaterally injected rats also in the contralateral amygdala. Healthy, well integrated transplants found in 6 out of 9 transplanted rats reduced the incidence of remote lesions (particularly in the contralateral hemisphere). Performance of individual animals reflected the state of the transplant. It is concluded that the impairment of spatial working memory is due not only to destruction of amygdala but also to diffuse damage of the limbic system. The slowly developing seizure-induced distant lesions can be partly prevented by embryonal grafts.

Amygdala↗
PubMed1997

Potentiation by DSP-4 of EEG slowing and memory impairment in basal forebrain-lesioned rats.

The effects of cholinergic and noradrenergic depletion, alone and in combination, on spatial memory and electroencephalogram (EEG) activity were investigated. Basal forebrain-lesioned rats exhibited a significant decrease in cortical choline acetyltransferase activity and spatial memory impairment. In the cortical EEG, the basal forebrain lesion induced EEG slowing such as an increase in delta power activity and a decrease in beta power activity. Noradrenergic depletion following a treatment with DSP-4 (N-2-(chloroethyl)-N-ethyl-2-bromobenzylamine) had no effect on cortical choline acetyltransferase activity and spatial memory, but it aggravated the cognitive impairment induced by the basal forebrain lesion. DSP-4 itself increased delta power activity in non-lesioned rats, whereas DSP-4 potentiated the EEG slowing induced by the basal forebrain lesions. Systemic administration of tetrahydroaminoacridine at 1 or 3 mg/kg, i.p., ameliorated the memory deficits and EEG slowing induced by the basal forebrain lesion. However, the drug could not attenuate the EEG slowing and memory impairment in rats that had received a combination of DSP-4 and basal forebrain lesion. These results suggest that noradrenergic depletion aggravated the EEG slowing and the spatial memory impairment induced by cholinergic dysfunction and may decrease the efficacy of an anticholinesterase agent in reversing the cortical cholinergic hypofunction.

Animals↗
PubMedDate not supplied

Firing characteristics of deep layer neurons in prefrontal cortex in rats performing spatial working memory tasks.

Single cells were recorded with 'tetrodes' in regions of the rat medial prefrontal cortex, including those which are targets of hippocampal afferents, while rats were performing three different behavioral tasks: (i) an eight-arm radial maze, spatial working memory task, (ii) a figure-eight track, delayed spatial alternation task, and (iii) a random food search task in a square chamber. Among 187 recorded units, very few exhibited any evidence of place-specific firing on any of the behavioral tasks, except to the extent that different spatial locations were related to distinct phases of the task. Furthermore, no prefrontal unit showed unambiguous spatially dependent delay activity that might mediate working memory for spatial locations. Rather, the cells exhibited diverse correlates that were generally associated with the behavioral requirements of performing the task. This included firing related to intertrial intervals, onset or end of trials, selection of specific arms on the eight-arm radial maze, delay periods, approach to or departure from goals, and selection of paths on the figure-eight track. Although a small number of cells showed similar behavioral correlates across tasks, the majority of cells showed no consistent correlate when recorded across multiple tasks. Furthermore, some units did not exhibit altered firing patterns in any of the three tasks, while others showed changes in firing that were not consistently related to specific behaviors or task components. These results are in agreement with previous lesion and behavioral studies in rats that suggest a prefrontal cortical role in encoding 'rules' (i.e. structural features) or behavioral sequences within a task but not in encoding allocentric spatial information. Given that the hippocampal projection to this cortical region is capable of undergoing LTP, our data lead to the hypothesis that the role of this projection is not to impose spatial representations upon prefrontal activity, but to provide a mechanism for learning the spatial context in which particular behaviors are appropriate.

Action Potentials↗
PubMed2005

Restoration of spatial working memory by genetic rescue of GluR-A-deficient mice.

Gene-targeted mice lacking the AMPA receptor subunit GluR-A (also called GluR1 encoded by the gene Gria1,) have deficits in hippocampal CA3-CA1 long-term potentiation (LTP) and have profoundly impaired hippocampus-dependent spatial working memory (SWM) tasks, although their spatial reference memory remains normal. Here we show that forebrain-localized expression of GFP-tagged GluR-A subunits in GluR-A-deficient mice rescues SWM, paralleling its rescue of CA3-CA1 LTP. This provides powerful new evidence linking hippocampal GluR-A-dependent synaptic plasticity to rapid, flexible memory processing.

Analysis of Variance↗