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At least 127 records · Page 7Linked to original sources

PubMed2001

Varieties of human spatial memory: a meta-analysis on the effects of hippocampal lesions.

The current meta-analysis included 27 studies on spatial-memory dysfunction in patients with hippocampal damage. Each study was classified on the basis of the task that was used, i.e., maze learning, working memory, object-location memory, or positional memory. The overall results demonstrated impairments on all spatial-memory tasks. Clear differences in effect size were found between positional memory on the one hand and maze learning, object-location memory, and working memory on the other hand. Lateralization was found only on maze learning and object-location memory. These findings clearly indicate that specific aspects of spatial memory can be affected in various degrees in patients with hippocampal lesions. Moreover, these results strongly support the notion that the hippocampus is important in the processing of metric positional information, probably in the form of an allocentric cognitive map.

Animals↗

PubMedDate not supplied

Effect of alpha lipoic acid, melatonin and trans resveratrol on intracerebroventricular streptozotocin induced spatial memory deficit in rats.

In the present study, the effect of antioxidants-alpha lipoic acid, melatonin and trans resveratrol were studied against intracerebroventricular streptozotocin induced spatial memory deficit. Male Wistar rats were injected with intracerebroventricular streptozotocin bilaterally. The rats were treated chronically with alpha lipoic acid (200 mg/kg, po), melatonin (20 mg/kg, ip) and trans resveratrol (20 mg/kg, ip) for 18 days starting from day 1 of streptozotocin injection in separate groups. The spatial memory was evaluated using the Morris water maze task. The intracerebroventricular streptozotocin rats treated with antioxidants showed significantly less spatial memory deficit both in the acquisition and probe trials as compared to the vehicle treated rats. The study demonstrated the effectiveness of alpha lipoic acid, melatonin and trans resveratrol in preventing spatial memory deficit induced by intracerebroventricular streptozotocin and it's potential in age related neurodegenerative disorders where oxidative stress is involved such as Alzheimer's disease.

Animals↗

PubMed1978

The effects of unilateral and bilateral ECT on verbal and visual spatial memory.

Investigated the effects of unilateral left (UL), unilateral right (UR), and bilateral (B) ECT on the performance of right-handed male patients on the Wechsler Memory Scale and two tests of the Williams battery, which provided eight independent measures of verbal memory and two of visual-spatial memory. Patients were tested three times: (1) within 1 week prior to ECT; (2) within 30 minutes after the sixth ECT; (3) 10 days after the sixty ECT. Double blind procedures were maintained carefully. Results showed a significant loss on second testing followed by a significant improvement 10 days later for all ECT groups compared with matched controls. There was some tendency for the UR group to show the least impairment on verbal measures and the UL group to show the least impairment on visual-spatial memory test of the WMS, but most of the differences between UL and UR groups and between each of these and the B group were not significant. The most sensitive test in differentiating among the ECT groups was the brief Verbal Learning subtest of the Williams battery.

Adult↗

PubMed2004

Reversible lesion of the rat's orbitofrontal cortex interferes with hippocampus-dependent spatial memory.

In this study, tetrodotoxin (TTX) inactivation was employed to evaluate the involvement of the rat's orbitofrontal cortex (OFC) in hippocampus-dependent spatial memory using Morris water maze (MWM) and place avoidance learning (PAL) tasks. In Experiment 1, rats trained in MWM task with two blocks of four trials per day for 3 consecutive days received bilateral injections of either TTX or saline into the OFC 60 min before each daily training session. The acquisition of spatial memory was evaluated 24h after the last training day and it was shown an impairment by the TTX. In Experiment 2, bilateral intra-OFC injections of TTX or saline were made immediately after two blocks of four trials. Testing 24h later, it was revealed that TTX also impairs spatial memory consolidation. In Experiments 3 and 4, rats were trained in a single 30-min session to avoid a 60 degrees segment of the stable circular (80-cm diameter) arena, entering which was punished by a mild shock (PAL task) and retention was tested 24h later in a 30-min extinction session. Bilateral injections of TTX or saline were made into the OFC 60 min before training or immediately after training. Again, TTX impaired the place avoidance retention when it was injected into the OFC either before (acquisition phase) or after (consolidation phase) training. These findings indicate that functional integrity of the OFC is necessary for both the acquisition and the consolidation of hippocampus-dependent spatial memory in rats.

Anesthetics, Local↗

PubMedDate not supplied

Anticholinergic sensitivity in the aging rat septohippocampal system as assessed in a spatial memory task.

The effects of central cholinergic blockade on spatial memory were tested in aged and basal forebrain-lesioned rats using the Morris Water Maze. In Experiment 1, aged rats (18-21 months old) were characterized as behaviorally impaired or nonimpaired based on water maze performance prior to an atropine sulfate challenge. In the atropine test (50 mg/kg, IP), both the impaired and the nonimpaired rats showed a severe disruption of their search behavior compared to young subjects. This effect was due to blockade of central receptors since peripheral cholinergic blockade using atropine methylbromide did not produce any impairments. Experiment 2 investigated effects of atropine on rats with septal lesions (SL), nucleus basalis lesions (NBL), and rats with both lesions combined (SL + NBL). Before drug treatment, the groups with septal lesions (SL and SL + NBL groups) displayed a moderate impairment in locating the platform site. However, similar to the aged rats, the septal-lesioned rats exhibited severe impairments in the water maze during atropine treatment. This effect was not seen in the normal controls or in the NBL rats. Aged rats, either impaired or nonimpaired in a spatial memory task, showed a pronounced sensitivity to pharmacological blockade of central cholinergic neurotransmission which resulted in severe deficits in spatial navigation in the water maze. Since the same behavioral deficit was produced by cholinergic blockade in young rats with septal lesions, we concluded that the impaired water maze performance seen in the aged rats during cholinergic blockade resulted from impaired function in the septohippocampal system.

Aging↗

PubMed2001

Age-independent and dose-response effects of ethanol on spatial memory in rats.

Results of previous studies have shown that ethanol impairs the acquisition of spatial memory in adolescent rats at doses below those required to impair the acquisition in adults. However, the previous work did not identify doses of ethanol that failed to impair acquisition in adolescents or that impaired acquisition in both adolescent and adult animals. This was our aim in the present study. Male, Long-Evans hooded rats (adolescent and adult) were treated intraperitoneally with 0.0, 0.5, or 2.5 g/kg of ethanol 30 min before daily training on a spatial or nonspatial version of the Morris water maze task. Twenty-four hours after training on the spatial task the animals were given a 1-min probe trial. The low dose of ethanol (0.5 g/kg) failed to impair the performance of animals from either age group on any tasks. It did, however, enhance the initial rate of acquisition on the spatial task. The 2.5-g/kg dose eliminated acquisition of spatial learning in animals of both ages and significantly attenuated performance on a nonspatial task in both age groups. However, the treatment effect in the nonspatial task was eliminated with controlling for baseline performance. These results establish a low dose of ethanol (0.5 g/kg) that does not impair acquisition of spatial memory in adolescent or adult rats. Moreover, the study findings show that 2.5 g/kg of ethanol markedly impairs acquisition of spatial memory in both adolescent and adult animals.

Aging↗

PubMed2005

Partial unilateral inactivation of the dorsal hippocampus impairs spatial memory in the MWM.

The hippocampus is one of the more widely studied structures related with spatial memory. In this study, we assessed the effect of unilateral inactivation of the dorsal hippocampus with tetrodotoxin (TTX) on the performance displayed by Wistar rats in the spatial version of the Morris water maze. In experiment 1, we injected into the dorsal hippocampus in two different groups of rats 1 microl of saline solution or 5 ng of TTX in 1 microl of saline each day immediately after the training during four consecutive days. This procedure blocked consolidation and impaired spatial memory in the TTX group. In experiment 2, a new group of subjects was trained in the Morris water maze for 8 days and was administered 1 microl of saline on day 7 (saline session) and TTX on day 8 (TTX session) into the dorsal hippocampus 40 min before the training. Only the treatment with TTX altered the retrieval of memories. These experiments showed that unilateral interventions on the dorsal hippocampus can affect consolidation as well as retrieval of well-established spatial memories.

Animals↗

PubMed2003

Intracerebroventricular injection of streptozotocin causes neurotoxicity to myelin that contributes to spatial memory deficits in rats.

It has been reported that intracerebroventricular (icv) injection of streptozotocin (STZ) impairs spatial memory by disrupting glucose utilization through an insulin-dependent mechanism in the cerebral cortex and hippocampus. However, evidence of septal damage and microglosis induced by icv STZ suggested that its neurotoxic effects could contribute to the memory impairment. The present study examined the histopathological changes in adult rats following three icv STZ injections (0.25 mg into each lateral ventricle) and their effects on spatial memory in a Morris water maze task. STZ retarded acquisition of reference learning (progressive reduction in escape latency) and disrupted working memory (difference in escape latency between the two swims within a daily session). STZ caused selective injury to myelin and axons in the fornix and hippocampus in association with activation of microglia. The 3rd ventricle was enlarged by 100-150% because of a loss of ependymal cells and damage to hypothalamic periventricular myelin but the process involved in these changes is unclear. Our findings provide an alternative explanation for the decrease in glucose utilization in the hippocampus and cortex and the impairment of spatial memory induced by STZ. These could result from a disruption of the communication through myelinated axons in the fornix connecting the septum and the hippocampus, and through other myelinated axons adjacent to the ventricles. The selective damage to myelin may well result from oxidative stress.

Animals↗

PubMed1991

Disproportionate incidental spatial-memory and recall deficits in amnesia.

Seventeen amnesics, including patients with Korsakoff's disease, post-encephalitic amnesia and amnesia caused by rupture of an anterior communicating artery aneurysm, were compared with 17 matched control subjects on a task in which 16 nameable shapes were placed on different squares of a 49-square grid. One version of the task tapped free recall and recognition of the shapes and a second version tapped three forms of spatial memory. The patients were tested after more learning opportunity and shorter delays than were the controls so as to match their recognition levels. Under these conditions, the amnesics performed worse than the controls on free recall, location-to-target memory, target-to-location memory and possibly on non-associative spatial memory although this was less impaired than target-to-location memory. Each of the main aetiological subgroups showed these disproportionate deficits to an apparently similar degree. The disproportionate free recall deficit was unrelated to the spatial memory deficits and overall severity of amnesia, and was associated with ageing and signs of frontal lobe dysfunction. The disproportionate spatial memory deficits were unrelated to frontal lobe dysfunction, but the target-to-location memory measure was associated with impairments of recognition and recall of target material. The results are broadly consistent with the context-memory deficit hypothesis of amnesia.

Adult↗

PubMed1996

Age-dependent spatial memory deficits in transgenic mice expressing the human mid-sized neurofilament gene: I.

Previous studies have revealed that the transgenic mouse line expressing the human neurofilament-mid-sized (NF-M) gene evidences age-dependent and cell-specific pathological neurofibrillary accumulation in the central nerve system. In the current study, we investigated the learning and memory processes of NF-M transgenic mice at 3 and 8 months of age in a modified Morris water maze using a series of tasks including those primarily related to reference memory (i.e., spatial learning, reversal learning and probe trials) and to working memory (i.e., matching to sample tasks with or without delays). At 3 months of age, NF-M transgenic mice were indistinguishable from age- and litter-matched non-transgenic wild-type controls on any of the tests of reference and working memory. At 8 months of age, however, the NF-M transgenic mice exhibited significantly poorer performance than the age- and litter-matched wild-type control mice on both reference and working memory tasks. Immunohistological study of the brains of the 8-month-old NF-M transgenic mice revealed spherical and tangle-like neurofilamentous accumulation in their cerebral cortices. These results suggest that NF-M transgenic mice express both age-related histopathological changes and age-dependent learning and memory deficits. Whether NF-M transgenic mice exhibit even more severe behavioral impairments when they become aged is currently under study.

Aging↗

PubMed1991

Intrahippocampal transplants of septal cholinergic neurons: high-affinity choline uptake and spatial memory function.

Recent studies have demonstrated that intrahippocampal cholinergic septal grafts can ameliorate deficits in spatial memory function and hippocampal cholinergic neurochemical activity in animals with disruptions of the septohippocampal system. However, no study has determined if the restoration of spatial memory function is correlated to the restoration of cholinergic activity, as measured by high-affinity choline uptake (HACU). The present study was designed to determine if such a correlation between behavioral and neurochemical restoration exists. Male Sprague-Dawley rats received either sham lesions (SHAM), bilateral lesions of the septohippocampal pathway (LES), or bilateral lesions along with intrahippocampal septal grafts (SG). After 8 months, rats were tested for their ability to perform spatial reference, spatial navigation and working memory tasks. Upon completion of the behavioral testing, neurochemical activity of the hippocampus was measured by HACU. The results indicate that animals in the SG group had significantly higher behavioral scores and hippocampal HACU rates than animals in the LES group. Regression analysis indicates that a significant correlation exists between performance on each behavioral task and HACU rates. These results demonstrate that hippocampal cholinergic activity, as measured by HACU, correlates significantly with performance on tests of spatial memory function.

Animals↗

PubMed1986

Thalamic role in spatial memory.

The contribution of structures in the limbic diencephalon to spatial memory function was investigated. Rats with lesions of either the anteroventral thalamus, anteromedial thalamus, dorsomedial thalamus or mammillary bodies were compared in their ability to perform a delayed alternation task. The results indicate the ablation of the thalamic nuclei did not impair delayed-alternation memory, but there was impairment following damage to the mammillary bodies. Placement of the discrete lesions was verified using Nissl sections and by tracing the pattern of projections using a silver degeneration stain. The results suggest that individual thalamic nuclei are not essential in the storage and/or retrieval of spatial memory. The data are discussed in terms of spatial deficits resulting from damage to the hippocampus proper or to the pathways connecting it to other brain structures.

Animals↗

PubMed2005

[From the abducens nucleus to spatial memory: an ocular motor journey].

Advances in our knowledge on eye movements over the last 25 years are reviewed, focusing on the author's experience. First, the advantages of binocular frontal vision, which is a common characteristic of all predator mammals, are compared to those of lateral vision, characterizing their preys. Binocular frontal vision implies a perfect parallelism of both eyes, which is ensured in the pons by means of the abducens nucleus, controlling abduction as well as adduction. The pathological example of the "one-and-a-half" syndrome, in which the abducens nucleus and the adjacent medial longitudinal fasciculus are simultaneously impaired, is described. The main brainstem syndromes involving vertical eye movements are also reviewed: in particular, the third nerve nucleus syndrome, in which both ipsilateral third nerve paralysis and contralateral superior rectus paralysis (with hypotropia) result from a unilateral third nerve nucleus lesion. A case of upbeat nystagmus (in the primary position of gaze) due to a small upper pontine lesion, probably affecting the ventral tegmental tract (VTT) is also reported. This is an opportunity to emphasize that, although a number of cases of upbeat nystagmus due to focal brainstem lesions affecting the upward vestibular pathway (UVP)--either at the upper pontine (VTT) or caudal medullary level--exist in the literature, no convincing cases with downbeat nystagmus (in the primary position of gaze) due to a focal brainstem lesion have been reported. Downbeat nystagmus could result from a UVP hyperactivity (secondary to a floccular lesion) and the notion that this pathway is physiologically predominant compared to the downward pathway, maybe due to gravity, is developed. A new hypothesis about the role of the caudal medulla in UVP is also proposed. Next, the cortical control of saccadic eye movements is reviewed, with a reminder that reflexive saccades are mainly triggered by the parietal eye field whereas intentional saccades depend upon the frontal eye field. The inhibition of reflexive saccades is mainly controlled by the dorsolateral frontal cortex (DLPFC), i.e. area 46 of Brodmann. A few examples of the use of saccades as a research tool and model in cognitive neurosciences are given. The use of memory-guided saccades allowed us to study spatial memory and led us to propose a relatively original conception of the cortical control of spatial memory in which the DLPFC, the parahippocampal cortex and the hippocampal formation could be involved successively according to specific periods of time. An experiment using functional magnetic resonance imaging in a paradigm studying decision is described, again with the involvement of the DLPFC in the decisional process. Lastly, the usefulness of eye movements in clinical neuro-ophthalmology at the bedside as well as in neurophysiological or even neuropsychological research in the laboratory is emphasized.

Abducens Nerve↗

PubMed1991

Differential effects of physostigmine and pilocarpine on the spatial memory deficits produced by two septo-hippocampal deafferentations in rats.

Rats that had received two kinds of septo-hippocampal deafferentations, medial septum (MS) lesion and fimbria-fornix (FF) transection, were assayed for brain cholineacetyltransferase (ChAT) activity and spatial memory in an 8-arm radial maze task. Both lesions produced profound and long-lasting spatial memory impairments, which were characterized by a reduction in the numbers of correct arm choices and first correct choices, a reduction in the percent of correct choices and an increase in the number of errors. The degree of memory impairment was severer in FF- than in MS-lesioned rats, and paralleled that of decreases in ChAT activity in the hippocampus. MS lesion reduced ChAT activity in the hippocampus by approximately 45%, while FF lesion almost completely depleted the activity. An intraperitoneal injection of physostigmine (0.0032-0.32 mg/kg), an acetylcholinesterase (AChE) inhibitor, significantly ameliorated the spatial memory deficit induced by MS lesion, but hardly affected that by FF lesion. In contrast, intraperitoneal doses (0.032-3.2 mg/kg) of pilocarpine, a muscarinic agonist, showed a significant improvement of both types of memory deficit with bell shaped dose-response curves. The drug was more potent in the FF- than in the MS-lesioned rats. These results suggest that the septo-hippocampal cholinergic system plays a crucial role in the maintenance of spatial memory, and that the degree of septo-hippocampal deafferentation affects the efficacy of cholinergic drugs.

Animals↗

PubMed2002

Intracerebral microinjections of delta 9-tetrahydrocannabinol: search for the impairment of spatial memory in the eight-arm radial maze in rats.

The purpose of this study was to identify brain sites that contribute to the delta(9)-tetrahydrocannabinol (delta(9)-THC)-induced impairment of spatial memory in rats. Rats were tested in the eight-arm radial maze after microinjections of delta(9)-THC into one of 14 different brain regions. The bilateral microinjection of delta(9)-THC (20 microg/side) impaired spatial memory when injected into the dorsal hippocampus (DH), ventral hippocampus (VH) or dorsomedial thalamus nucleus (DMT). However, rats treated with delta(9)-THC into DMT produced preseverative behavior which has not been observed by systemic administration of delta(9)-THC. On the other hand, spatial memory was unaffected by microinjections of delta(9)-THC into the other 11 areas examined: frontal (FC) and frontoparietal (FPC) cortex, central (ACE) and basolateral (ABL) amygdaloid nucleus, medial caudate putamen (CPM), lateral hypothalamus (LH), mammillary body (MB), basal forebrain (BF), medial septal nucleus (SEP) and dorsal (DR) and median (MR) raphe nucleus. These results suggest that DH and VH may be important brain sites for the delta(9)-THC-induced impairment of spatial memory.

Animals↗

PubMed1996

Redistribution of spatial representation in the hippocampus of aged rats performing a spatial memory task.

Young and old rats performed on a maze according to a forced-choice and then a spatial memory procedure either in the same or a different environment. Aged rats were slower to learn the spatial memory task when tested in the same, but not in a different, room. One interpretation of this pattern of results is that although old rats learn new rules as quickly as young rats, they show less flexibility with old rules and familiar spatial information. Impaired choice accuracy during asymptote performance suggests poor processing of trial-unique information by old rats. Spatial correlates of hippocampal CA1 and hilar cells varied with task demand: CA1 cells of aged rats showed more spatially selective place fields, whereas hilar cells showed more diffuse location coding during spatial memory, and not forced-choice, tests. Such representational reorganization may reflect a compensatory response to age-related neurobiological changes in hippocampus.

Aging↗

PubMed2006

Effect of levetiracetam on visual-spatial memory following status epilepticus.

Status epilepticus (SE) is often followed by severe cognitive impairment, including memory impairment. Previous studies have shown that SE is associated with impairment of single cells in the hippocampus that fire action potentials when the animal is in a specific location in space, the so-called place cells, and that place cell function correlates well with performance in tasks of visual-spatial memory. Place cell patterns therefore appear to be an excellent measure of spatial memory and may serve as a tool to assess seizure-induced impairment in memory. In this study we determined the relationship between visual-spatial memory and place cell function following SE. In addition, we determined if levetiracetam (LEV), an antiepileptic drug with a novel mechanism of action, can improve cognitive function and place cell firing patterns when administered following SE. SE was induced in adult male rats which were then randomized to post-SE treatment with LEV or normal saline (NS) treatment for 14 days. Non-SE control rats also were randomized to LEV or NS. Following discontinuation of LEV rats were tested for visual-spatial memory in the Morris water-maze and then underwent unit recording in the CA1 region of the hippocampus. Brains were then evaluated for cell loss and mossy fiber sprouting. SE was associated with severely impaired performance in the water-maze with SE rats demonstrating no learning over four days of testing. Paralleling this memory deficit was a marked disturbance in firing patterns of pyramidal neurons in CA1. Non-SE rats learned quickly over four days of water-maze testing and had normal pyramidal cell firing patterns. LEV had no major effects on water-maze performance or place cell function. Histopathological examination of the brains showed severe cell loss in CA1 in all of the SE rats with lesser degrees of injury in CA3 and the hilus. LEV treatment resulted in less histological damage in the hippocampus but had no effect on visual-spatial function or place cell physiology in either control or SE rats.

Animals↗

PubMed2004

The serotonin1A receptor agonist 8-OHDPAT reverses delta 9-tetrahydrocannabinol-induced impairment of spatial memory and reduction of acetylcholine release in the dorsal hippocampus in rats.

We studied the effects of 8-hydroxy-2-(di-n-propylamino)tetralin (8-OHDPAT), a 5-HT1A receptor agonist, on both delta9-tetrahydrocannabinol-induced spatial memory impairment in an 8-arm radial maze, and the reduction of acetylcholine release in the dorsal hippocampus as assessed by in vivo microdialysis in rats. A 6 mg/kg i.p. dose of delta9-tetrahydrocannabinol impaired spatial memory in the 8-arm radial maze and decreased the acetylcholine release in the dorsal hippocampus. 8-OHDPAT, at very low doses of 0.1-0.3 microg/kg, reversed both the impairment of spatial memory and the decrease in acetylcholine release induced by delta9-tetrahydrocannabinol. These findings suggest that low doses of 8-OHDPAT may improve delta9-tetrahydrocannabinol-induced impairment of spatial memory by enhancing acetylcholine release in the dorsal hippocampus.

8-Hydroxy-2-(di-n-propylamino)tetralin↗