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Results for “Spatial memory”

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PubMed1985

Dissociation between components of spatial memory in rats after recovery from the effects of retrohippocampal lesions.

A series of 4 experiments examined the performance of rats with retrohippocampal lesions on a spatial water-maze task. The animals were trained to find and escape onto a hidden platform after swimming in a large pool of opaque water. The platform was invisible and could not be located using olfactory cues. Successful escape performance required the rats to develop strategies of approaching the correct location with reference solely to distal extramaze cues. The lesions encompassed the entire rostro-caudal extent of the lateral and medial entorhinal cortex, and included parts of the pre- and para-subiculum, angular bundle and subiculum. Groups ECR 1 and 2 sustained only partial damage of the subiculum, while Group ECR+S sustained extensive damage. These groups were compared with sham-lesion and unoperated control groups. In Expt 1A, a profound deficit in spatial localisation was found in groups ECR 1 and ECR+S, the rats receiving all training postoperatively. In Expt 1B, these two groups showed hyperactivity in an open-field. In Expt 2, extensive preoperative training caused a transitory saving in performance of the spatial task by group ECR 2, but comparisons with the groups of Expt 1A revealed no sustained improvement, except on one measure of performance in a post-training transfer test. All rats were then given (Expt 3) training on a cueing procedure using a visible platform. The spatial deficit disappeared but, on returning to the normal hidden platform procedure, it reappeared. Nevertheless, a final transfer test, during which the platform was removed from the apparatus, revealed a dissociation between two independent measures of performance: the rats with ECR lesions failed to search for the hidden platform but repeatedly crossed its correct location accurately during traverses of the entire pool. This partial recovery of performance was not (Expt 4) associated with any ability to discriminate between two locations in the pool. The apparently selective recovery of aspects of spatial memory is discussed in relation to O'Keefe and Nadel's (1978) spatial mapping theory of hippocampal function. We propose a modification of the theory in terms of a dissociation between procedural and declarative subcomponents of spatial memory. The declarative component is a flexible access system in which information is stored in a form independent of action. It is permanently lost after the lesion. The procedural component is "unmasked" by the retrohippocampal lesion giving rise to the partial recovery of spatial localisation performance.

Animals↗

PubMed2006

Spatial memory formation and memory-enhancing effect of glucose involves activation of the tuberous sclerosis complex-Mammalian target of rapamycin pathway.

The tuberous sclerosis complex-mammalian target of rapamycin (TSC-mTOR) cascade integrates growth factor and nutritional signals to regulate the synthesis of specific proteins. Because both growth factor signaling and glucose have been implicated in memory formation, we questioned whether mTOR activity is required for long-term spatial memory formation and whether this cascade is involved in the memory-augmenting effect of centrally applied glucose. To test our hypothesis, we directly administered rapamycin (an inhibitor of mTOR), glucose, 5-aminoimidazole-4-carboxamide-1beta-4-ribonucleoside (AICAR; an activator of AMP kinase), or glucose plus rapamycin into the dorsal hippocampus after we trained rats in the Morris water maze task. The results from these studies indicate that glucose enhances, whereas AICAR and rapamycin both impair, long-term spatial memory. Furthermore, the memory-impairing effect of targeted rapamycin administration could not be overcome by coadministration of glucose. Consistent with these behavioral results, biochemical analysis revealed that glucose and AICAR had opposing influences on the activation of the TSC-mTOR cascade, as indicated by the phosphorylation of ribosomal S6 kinase (S6K) and 4E binding protein 1 (4EBP1), targets of mTOR. Together, these findings suggest that memory formation requires the mTOR cascade and that the memory-enhancing effect of glucose involves its ability to activate this pathway.

Aminoimidazole Carboxamide↗

PubMedDate not supplied

Intraretrosplenial cortical grafts of fetal cholinergic neurons and the restoration of spatial memory function.

The retrosplenial cortex (RSC) receives cholinergic afferent fibers from the medial septal nucleus and diagonal band of Broca (DBB) by way of the cingulate bundle and the fornix. Bilateral lesions of both the cingulate and fornix pathways result in a complete depletion of cholinergic input to the RSC. In the present study we have examined the effects of transplanting cholinergic neurons from fetal rat pups to the RSC of adult rats following lesions of the cingulate bundle and fornix. The animals with lesions exhibited severe spatial memory impairments with a complete loss of extrinsic cholinergic afferents to the RSC. Animals with intraretrosplenial cortical transplants exhibited significant improvements in learning and memory performance as revealed by decreased escape latencies in spatial reference memory tests, increased numbers of platform crossings in spatial navigation tests, and a higher percentage of correct choices in a spatial working memory task. These improvements appeared to be cholinergically mediated because atropine administration significantly disrupted spatial navigation performance. The survival of the transplanted cholinergic neurons and their innervation of the RSC were characterized using a monoclonal antibody to choline acetyltransferase (ChAT). The staining of graft-derived ChAT-positive fibers also revealed a pattern of innervation that mimicked that of the cholinergic input in normal animals. These results indicate that intraretrosplenial cortical transplants of cholinergic neurons can rectify spatial memory deficits produced by the loss of intrinsic cholinergic afferents from the medial septal nucleus.

Animals↗

PubMed2003

Effect of nilvadipine on the cerebral ischemia-induced impairment of spatial memory and hippocampal apoptosis in rats.

We investigated the effects of nilvadipine and amlodipine on the cerebral ischemia-induced impairment of spatial memory in 8-arm radial maze performance and hippocampal CA1 apoptosis in rats. Single cerebral ischemia impaired memory without inducing apoptosis. In these rats, neither nilvadipine nor amlodipine at 3.2 mg/kg, i.p. improved the impaired memory. On the other hand, repeated cerebral ischemia (10 min ischemia x 2, 1 h interval) impaired spatial memory and induced hippocampal apoptosis 7 days after the final occlusion/reperfusion. Moreover, repeated ischemia increased the apoptotic cell number, an effect observed after 3 days and peaked after 7 days. However, mRNA expression of the apoptosis-related early oncogene bax and CPP 32 (caspase-3) was observed after 24 h. In these rats, nilvadipine, but not amlodipine, significantly improved memory, concomitantly decreased hippocampal apoptosis, and suppressed both bax and CPP 32 expression. These results suggest that nilvadipine improved the memory impairment in repeated ischemia by reducing bax and CPP 32 expression and suppressing the induction of apoptosis in the hippocampus. Nilvadipine may have a neuroprotective effect and could be a useful pharmacotherapeutic agent for cerebrovascular dementia.

Animals↗

PubMed2004

Are spatial memories strengthened in the human hippocampus during slow wave sleep?

In rats, the firing sequences observed in hippocampal ensembles during spatial learning are replayed during subsequent sleep, suggesting a role for posttraining sleep periods in the offline processing of spatial memories. Here, using regional cerebral blood flow measurements, we show that, in humans, hippocampal areas that are activated during route learning in a virtual town are likewise activated during subsequent slow wave sleep. Most importantly, we found that the amount of hippocampal activity expressed during slow wave sleep positively correlates with the improvement of performance in route retrieval on the next day. These findings suggest that learning-dependent modulation in hippocampal activity during human sleep reflects the offline processing of recent episodic and spatial memory traces, which eventually leads to the plastic changes underlying the subsequent improvement in performance.

Adult↗

PubMed2003

Deficient spatial memory induced by blockade of beta-adrenoceptors in the hippocampal CA1 region.

A previous study showed that intra-CAl infusion of the beta-adrenergic antagonist DL-propranolol interfered with consolidation of memory for contextual fear conditioning (J.-Z. Ji, X.-M. Wang, & B.-M. Li, 2003). The present study investigated the effect of similarly administered DL-propranolol on consolidation of spatial memory for the water maze. DL-propranolol infused 5 min, but not 6 hr, posttraining caused a deficit in 48-hr memory for the spatial water maze task, whereas similarly administered D-propranolol, which has an equipotent "local-anesthetic" activity but significantly lower beta-blocking activity, induced no amnesia. However, DL-propranolol administered 5 min posttraining did not impair 48-hr memory for the cued water maze task. Thus, beta-adrenoceptor in area CA1 is involved in regulating consolidation of spatial memory for the water maze.

Adrenergic beta-Antagonists↗

PubMed2006

Influence of predator stress on the consolidation versus retrieval of long-term spatial memory and hippocampal spinogenesis.

We have studied the influence of predator stress (30 min of cat exposure) on long-term (24 h) spatial memory and the density of spines in basilar dendrites of CA1 neurons. Predator stress occurred either immediately before water maze training (Stress Pre-Training) or before the 24 h memory test (Stress Pre-Retrieval). The Control (nonstress) group exhibited excellent long-term spatial memory and a robust increase in the density of stubby, but not mushroom, shaped spines. The Stress Pre-Training group had impaired long-term memory and did not exhibit any changes in spine density. The Stress Pre-Retrieval group was also impaired in long-term memory performance, but this group exhibited an increase in the density of stubby, but not mushroom, shaped spines, which was indistinguishable from the control group. These findings indicate that: (1) A single day of water maze training under control conditions produced intact long-term memory and an increase in the density of stubby spines in CA1; (2) Stress before training interfered with the consolidation of information into long-term memory and suppressed the training-induced increase in spine density; and (3) Stress immediately before the 24 h memory test trial impaired the retrieval of the stored memory, but did not reverse the training-induced increase in CA1 spine density. Overall, this work provides evidence of structural plasticity in dendrites of CA1 neurons which may be involved in the consolidation process, and how spinogenesis and memory are modulated by stress.

Amnesia↗

PubMed2002

The perirhinal cortex and long-term spatial memory in rats.

Two experiments examined the effects of perirhinal cortex and hippocampal neurotoxic lesions on the retention of allocentric information. Perirhinal (Expt. 1) and hippocampal rats (Expt. 2) were trained on an allocentric task until they reached a performance equal to that of the control groups. Results showed that 24 days after acquisition, during a retraining period, only the hippocampal rats presented a deficit in retention. These results suggest that the perirhinal cortex and the hippocampus can be functionally dissociated in terms of their participation in the formation of long-term spatial memory. Also, the allocentric spatial memory functions of the hippocampus seem not to depend on their afferent connections with the perirhinal cortex.

Animals↗

PubMed1997

Pigs in space: spatial memory and its susceptibility to interference.

This study provided basic information about spatial memory in the domestic pig, Sus scrofa and examined how susceptible it is to disruption by environmental stimuli. Eight male pigs were tested individually in a foraging arena. Each day, they entered the arena to search for food randomly located in one of 10 enclosed areas (search trial). After finding and eating the food, they were removed from the arena for a retention interval, and then allowed back in to relocate the food in the same area as previously (relocation trial). Once pigs had achieved a criterion level of performance in relocation trials, 'disturbances' (e.g. isolation, novel food source, novel spatial environment) were presented during the retention interval. Disturbance days were separated by control days on which no disturbance was presented. During search trials, pigs did not use food-related cues to locate food, but appeared to use memory to search systematically and avoid revisits to empty areas. During relocation trials, they found food using fewer area visits than expected by chance, indicating that they could remember the location of food across both 10-min and 2-h retention intervals. Disturbances administered during 10-min retention intervals resulted in more relocation errors than on corresponding control days, indicating that spatial memory in pigs is susceptible to interference by relatively mild environmental stimuli, in contrast to that in rats, Rattus norvegicus and pigeons, Columba livia which appears to be highly resistant to retroactive interference even when potent stimuli are used. Analysis of error locations suggested that disturbances probably acted to increase the general area in which the pig remembered the food to be located, and so reduced accuracy of memory without eradicating it. There was no evidence that errors made during relocation trials represented sampling of areas not visited during the preceding search trial.Copyright 1997 The Association for the Study of Animal Behaviour

Journal Article↗

PubMed2006

Thiamine deficiency decreases glutamate uptake in the prefrontal cortex and impairs spatial memory performance in a water maze test.

Using an animal model of Wernicke-Korsakoff syndrome, in which rats were submitted to a chronic ethanol treatment with or without a thiamine deficiency episode, the glutamate uptake in the prefrontal cortex and spatial memory aspects were studied. It was found that (i) thiamine deficiency, but not chronic ethanol consumption, induced a significant decrease of glutamate uptake; (ii) thiamine-deficient subjects showed an impaired performance in the water maze spatial memory test though these animals were able to learn the task during the acquisition. In spite of the fact that thiamine deficiency affects both glutamate uptake and spatial reference memory, there was no significant correlation between these two data. The present results show that, although prefrontal cortex is considered by some authors a not vulnerable area to lesions caused by thiamine deficiency, this vitamin deficiency does cause a neurochemistry dysfunction in that region.

Animals↗

PubMed1990

Selective activation effects of concurrent verbal and spatial memory loads in left-handed and right-handed adults.

Thirty-two left-handed subjects, divided into four groups according to sex and familial sinistrality, and 16 right-handed subjects without familial sinistrality (8 male, 8 female) participated in a tachistoscopic unilateral letter-identification task with concurrent verbal- and spatial-memory loads. Across groups, a significant right visual field advantage for letter-identification was found. In the majority of both left-handed and right-handed subjects, the concurrent verbal-memory load resulted in a selective activation, with the right visual field performance showing improvement. However, the group of left-handed males with a positive family history of sinistrality gave less evidence of selective left-hemispheric activation as a consequence of the verbal-memory load. The concurrent spatial-memory load did not result in a consistent pattern of selective activation.

Adolescent↗

PubMed2002

Chronic ethanol consumption induces tolerance to the spatial memory impairing effects of acute ethanol administration in rats.

A large number of studies in rats have investigated the effects of acute and chronic ethanol administration on performance on many spatial learning and memory tasks. However, no study has addressed the problem of whether chronic ethanol consumption induces tolerance to acute ethanol-induced spatial memory deficits. In this study, we analyzed the behavioral effects of acute ethanol administration on spatial memory and locomotor activity in rats chronically intoxicated by ethanol. Male Sprague-Dawley rats were given as their only available liquid source a 10% (v/v) aqueous ethanol solution for 2 weeks before behavioral testing and during the 1-week behavioral testing period. They were treated intraperitoneally with 1.5 g/kg of ethanol 30 min before daily training in the Morris water maze, a spatial memory task sensitive to hippocampal damage. Our results demonstrate that learning and spatial memory of ethanol-consuming animals were not altered compared with control rats. Chronic ethanol consumption had no effect on spatial reference memory in terms of either the distance traveled to find the hidden platform during the acquisition phase of the experiment, or the time spent in the training quadrant during the retention trial. Acute ethanol administration impaired spatial memory in control rats and this impairment was reversed in chronic ethanol-consuming animals, revealing that chronic ethanol consumption did induce tolerance to the spatial memory deficits induced by acute ethanol injection, although plasma ethanol levels did not differ between the two groups. In contrast, chronic ethanol consumption did not induce tolerance to the acute ethanol-induced stimulatory locomotor activity measured in the same animals. Our results, therefore, indicate that chronic ethanol consumption induces tolerance to the cognitive impairing effects, but not to the locomotor stimulatory effects of acute ethanol administration in rats, suggesting that these two behavioral effects of ethanol do not share a common mechanism in the CNS.

Alcohol Drinking↗

PubMed1991

Neonatal anoxia induces transitory hyperactivity, permanent spatial memory deficits and CA1 cell density reduction in developing rats.

Physical and reflex development, spontaneous behavior in open field and spatial memory abilities have been studied in rats after neonatal anoxia. Histological analysis of the hippocampal fields have been carried out in selected animals at the end of the testing period. No differences between control and anoxic rats were recorded in the physical and reflex development. Hyperactivity in open field was present in anoxic animals only transiently between P20 and P45. Spatial memory abilities, tested at two developmental stages by means of a maze and a water maze, appeared to be defectual not only during the hyperactivity period but also in adulthood. The histological analysis of the different hippocampal fields demonstrated a significant difference between anoxic and control rats in the cell density of the CA1 field. The present data demonstrate that neonatal anoxia, besides determining only transitory defects in open field behavior, profoundly affects cognitive abilities and cell density in CA1 hippocampal field. These results might be of relevance in the interpretation of the substrate of the cognitive impairment seen in hyperactive children that are exposed to hypoxia at birth.

Animals↗

PubMed1994

Steroid hormone influences on spatial memory.

Our studies have shown that both stress-induced, enhanced secretion of corticosterone and adrenalectomy-induced, reduced secretion of corticosterone are associated with impaired spatial memory performance. On the other hand, estradiol administration is associated with enhancements in spatial memory performance. Although these changes in performance are small, they are consistent with structural changes induced by these hormones (or their lack) on specific cells within the hippocampus which form the tri-synaptic loop (a summary of the behavioral and morphological effects is shown in Figs. 1 and 2). Thus, these results suggest that the morphological changes induced by the hormones have an impact on hippocampal function. Important goals of future studies are to seek ways to maximize gonadal hormone-dependent enhancements in memory function and to minimize adrenal steroid-dependent impairments in memory function as well as to understand the mechanisms behind these behavioral and morphological changes.

Animals↗

PubMed1997

The effects of type I and type II corticosteroid receptor agonists on exploratory behavior and spatial memory in the Y-maze.

We investigated the effects of two adrenal steroid agonists on adrenalectomized (ADX) rats' performance on the Y-maze. The Y-maze was chosen because memory can be assessed quickly and because it is sensitive to various parameters of exploratory behavior and spatial memory performance. Four days after surgery, ADX rats were injected with aldosterone (ALDO, a selective Type I receptor agonist), RU362 (a selective Type II receptor agonist) or sesame vehicle at three different time points (120 min prior to Trial 1, immediately after Trial 1 or 120 min after Trial 1). SHAM-operated rats injected with vehicle were also tested. The results indicate that vehicle-treated ADX rats were impaired on spatial recognition memory compared to SHAM rats. Treatment with ALDO restored spatial recognition memory performance of ADX rats to a level comparable to SHAM-treated rats by acting on acquisition and consolidation, whereas treatment with RU362 did not change the poor spatial recognition memory performance of ADX rats. Discrimination memory was improved only when either agonist was injected prior to the first trial, strongly suggesting a non-selective effect of corticosteroids on discrimination memory such as increasing arousal. A detailed analysis of exploratory behavior showed that both the ALDO- and RU362-treated rats explored the Y-maze more than the ADX and SHAM groups at all periods of the experiment. These results show that the non-specific increase in exploratory behavior induced by replacing corticosteroids targeted at Type I and Type II receptors was used differentially with the ALDO-treated rats learning and consolidating spatial information better than the RU362-treated rats. These data are discussed along with other evidence to suggest that Type II receptors may require the simultaneous occupancy of Type I receptors to affect learning and memory processes.

Adrenalectomy↗

PubMed1994

Lack of effect of lesions in the anterior cingulate cortex and retrosplenial cortex on certain tests of spatial memory in the rat.

The effects of cytotoxic lesions in either the anterior cingulate cortex or the retrosplenial cortex were compared with those of fornix lesions on three tests of spatial memory. Two of the tasks, delayed nonmatching-to-position and spatial reversal learning, were tested in an automated apparatus. The third task, forced alternation, was tested in a T-maze. Neither anterior cingulate nor retrosplenial cortex damage produced any significant impairment on the three tasks. In contrast, rats with fornix lesions (hippocampal system damage) were markedly impaired on all three tasks. The results, which were considered in the light of proposals for a hippocampal--anterior thalamic--cingulate system that is important for spatial memory, suggest that neither of the cingulate regions involved in this study form a critical subcomponent of this proposed system. It is therefore assumed that the cingulate cortices are only critical for certain classes of spatial problem. It is also suggested that in some previous studies the effects of inadvertent damage to the cingulum bundle may have contributed to the apparent effects of cingulate lesions.

Animals↗

PubMed2006

Effects of chronic noise stress on spatial memory of rats in relation to neuronal dendritic alteration and free radical-imbalance in hippocampus and medial prefrontal cortex.

Spatial memory is coordinated with different brain regions especially hippocampus (HIP) and medial prefrontal cortex (mPFC). Influence of noise stress on working and reference memory error in rats was evaluated by radial eight-arm maze experiment. Changes in the dendritic count were observed in the brain regions such as CA1, CA3 regions of HIP and layers II, III of mPFC. In order to understand the possible mechanism behind noise stress-induced changes, free radical status and acetylcholinesterase (AChE) activity in HIP and mPFC were evaluated. Plasma corticosterone level was also evaluated. Results obtained in this study showed that after noise-stress exposure, 100 dBA/4h per day for 30 days, working and reference memory error increased significantly (P < 0.05) when compared to control animals. Neuronal dendritic count in the HIP was reduced in the 2nd and 3rd order dendrites but not in the mPFC. Superoxide dismutase, lipid peroxidation, plasma corticosterone level and AChE activity were significantly increased in the 1 day, 15 days and 30 days stress groups animal significantly. Catalase and glutathione peroxidase activity were increased in the 1 day and 15 days noise-stress groups but decreased in the 30 days noise-stress group and GSH level was decreased in all the stress exposed animals. In conclusion, oxidative stress, increased AChE activity, reduced dendritic count in HIP, mPFC regions and elevated plasma corticosterone level which develops in long-term noise-stress exposed rats, might have caused the impairment of spatial memory.

Animals↗

PubMed2004

Impaired acquisition of spatial memory 2 weeks after isoflurane and isoflurane-nitrous oxide anesthesia in aged rats.

Aged rats are impaired on a spatial memory task for at least 24-48 h after isoflurane-nitrous oxide anesthesia. In this study, we tested how long the impairment lasts and investigated the role of nitrous oxide. Eighteen-month-old rats were randomized to anesthesia for 2 h with 1.2% isoflurane with or without 70% nitrous oxide or a control group (30% oxygen). Two weeks later, rats were tested daily for 14 days on a 12-arm radial maze. The number of correct choices to first error, total errors, and time to complete the maze were recorded. Rats anesthetized with 1.2% isoflurane with 70% nitrous oxide made fewer correct choices before first error (P < or = 0.05). Trends toward similar results were noted for error rate and time to complete the maze, but these did not achieve statistical significance. Post hoc analysis comparing all anesthetized rats to controls demonstrated that anesthetized rats made fewer correct choices to first error (P < or = 0.05) and took longer to complete the maze (P <or = 0.05). There were no differences in total number of errors (P < or = 0.06). Thus, spatial memory is impaired for 2 wk after general anesthesia in aged rats independent of whether nitrous oxide is used.

Aging↗