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Results for “Spatial memory”

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PubMed1998

Psychomotor and spatial memory performance in aging male Fischer 344 rats.

Psychomotor and spatial memory performance were examined in male Fischer 344 rats that were 6, 12, 15, 18, and 22 months of age, to assess these parameters as a function of age and to determine at what age these behaviors begin to deteriorate. Complex motor behaviors, as measured by rod walk, wire suspension, plank walk, inclined screen, and accelerating rotarod performance, declined steadily with age, with most measures being adversely affected as early as 12 to 15 months of age. Spatial learning and memory performance, as measured by the working memory version of the Morris water maze (MWM), showed decrements at 18 and 22 months of age (higher latencies on the working memory trial), with some change noticeable as early as 12-15 months of age (no improvement on the second trial following a 10-min retention interval); these differences were not due to swim speed. Therefore, complex motor and spatial memory behaviors show noticeable declines early in the lifespan of the male Fisher 344 rat. This cross-sectional age analysis study using the latest behavioral techniques determines the minimal age at which psychomotor and spatial learning and memory behaviors deteriorate; this information is important when planning for longitudinal studies where interventions are tested for their efficacy in preventing or restoring age-related behavioral deficits.

Aging↗

PubMed2000

Effect of histamine H3-receptor antagonist clobenpropit on spatial memory of radial maze performance in rats.

AIM: The effect of histamine H3-receptor antagonist, clobenpropit (VUF9153) on spatial memory deficits induced by scopolamine was investigated in rats. METHODS: Eight-Arm radial maze performance was used to measure spatial memory in rats, and the brain regions were subsequently dissected and histamine contents were determined by HPLC. RESULTS: Intracerebroventricular (icv) injection of clobenpropit (50 micrograms) ameliorated memory impairment induced by scopolamine in both parameters of radial maze performance. The amelioration induced by clobenpropit was antagonized by an H3-agonist, (R)-alpha-methylhistamine (5-10 micrograms). alpha-Fluoromethylhistidine (10, 20 micrograms), a histidine decarboxylase inhibitor, also effectively reversed clobenpropit-induced ameliorating effects. CONCLUSION: The brain histamine H3-receptor antagonists are highly related to the spatial memory, and this action may be due to cholinergic neurons.

Animals↗

PubMed1996

Deferoxamine improves spatial memory performance following experimental brain injury in rats.

Traumatic brain injury (TBI) causes impairments of both motor and spatial memory performances. Research is only beginning to reveal the biochemical mechanism(s) underlying these deficits. It has been postulated that reactive oxygen species such as the superoxide and hydroxyl radicals, as well as the peroxynitrite anion, are generated by injury and may play a critical role in the observed memory deficits. The highly reactive hydroxyl radical, which is thought to contribute to neuronal toxicity, can be generated by an iron-catalyzed reaction. The source of this iron (or iron-bound proteins) could be a compromise of the blood-brain barrier, which can occur following TBI. In this report, we investigate the ability of deferoxamine, a scavenger of free iron, the hydroxyl radical and the peroxynitrite anion, to facilitate behavioral recovery following a controlled cortical impact of rats. Intraperitoneal administration of this drug prior to the injury did not affect the rate of recovery from motor deficits in comparison to vehicle (saline)-injected animals. However, deferoxamine-treated animals showed significant improvement in spatial memory performance in a Morris water maze task. Volumetric analysis of cortical tissue loss showed no significant differences between vehicle- and drug-injected animals. Similarly, histological examination of the hippocampus did not reveal any gross differences between the two groups. These results indicate that deferoxamine improves spatial memory performance, possibly through protection from neuronal dysfunction.

Animals↗

PubMed2003

The stress experience dependent long-term depression disassociated with stress effect on spatial memory task.

Behavioral stress can either block or facilitate memory and affect the induction of long-term potentiation (LTP) and long-term depression (LTD). However, the relevance of the stress experience-dependent long-term depression (SLTD) to spatial memory task is unknown. Here we have investigated the effects of acute and sub-acute elevated platform (EP) and foot shock (FS) stress on LTD induction in CA1 region of the hippocampus of anesthetized rats and spatial memory in Morris water maze. We found that LTD was facilitated by acute EP stress, but not by sub-acute EP stress that may be due to the fast adaptation of the animals to this naturalistic mild stress. However, FS stress, an inadaptable strong stress, facilitated LTD induction both in acute and sub-acute treatment. In addition, with the same stress protocols, acute EP stress impaired spatial memory but the sub-acute EP stressed animals performed the spatial memory task as well as the controls, may due to the same reason of adaptation. However, acute FS stress slightly impaired learning but sub-acute FS even enhanced memory retrieval. Our results showed that SLTD was disassociated with the effect of stress on memory task but might be related to stress experience-dependent form of aberrant memory.

Adaptation, Biological↗

PubMed2004

Frames of reference in spatial memories acquired from language.

Four experiments examined reference systems in spatial memories acquired from language. Participants read narratives that located 4 objects in canonical (front, back, left, right) or noncanonical (left front, right front, left back, right back) positions around them. Participants' focus of attention was first set on each of the 4 objects, and then they were asked to report the name of the object at the location indicated by a direction word or an iconic arrow. The results indicated that spatial memories were represented in terms of intrinsic (object-to-object) reference systems, which were selected using egocentric cues (e.g., alignment with body axes). Results also indicated that linguistic direction cues were comprehended in terms of egocentric reference systems, whereas iconic arrows were not.

Cues↗

PubMed2005

Sequestration of serum response factor in the hippocampus impairs long-term spatial memory.

The formation of long-term memory has been shown to require protein kinase-mediated gene expression. One such kinase, mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK), can lead to the phosphorylation of serum response factor (SRF) and Elk-1, enhancing the expression of target genes. However, a direct involvement of these transcription factors in memory storage has not been demonstrated. We have employed an oligonucleotide decoy technique to interrogate SRF and Elk-1. Previously, it has been shown that intra-amygdalal infusion of small double-stranded decoy oligonucleotides for nuclear factor-kappaB (NFkappaB) can impair long-term memory for fear-potentiated startle. Using this approach, we found that intra-hippocampal infusion of NFkappaB decoy oligonucleotides also impairs long-term spatial memory, consistent with a role for this factor in long-term memory storage. Decoy oligonucleotides containing the binding site for SRF, as confirmed by shift-western, did not influence memory acquisition but impaired long-term spatial memory. Analysis of search behavior during the transfer test revealed deficits consistent with a loss of precise platform location information. In contrast, oligonucleotides with a binding site for either Elk-1 or another target of ERK activity, SMAD3/SMAD4, did not interfere with memory formation or storage. These findings suggest that SRF-mediated gene expression is required for long-term spatial memory.

Animals↗

PubMed2006

The nootropic and neuroprotective proline-containing dipeptide noopept restores spatial memory and increases immunoreactivity to amyloid in an Alzheimer's disease model.

The effects of the novel proline-containing nootropic and neuroprotective dipeptide, noopept (GVS-111, N-phenylacetyl-L-prolylglycine ethyl ester) were investigated in NMRI mice following olfactory bulbectomy. We have shown previously that these animals developed Alzheimer's disease (AD)-like behaviour, morphology and biochemistry including impairment of spatial memory, regional neuronal degeneration and elevated Abeta peptide brain levels. In the current investigation, spatial memory was assessed using the Morris water maze and serum antibodies to in vitro morphologically characterized amyloid structures of both Abeta((25-35)) peptide and equine lysozyme, as well as to neurotrophic glial factor S100b, were analyzed by enzyme-linked immunosorbent assay (ELISA). Noopept (administered at a dose of 0.01 mg/kg for a period of 21 days and during a further 5 days training) restored spatial memory and increased serum antibody levels to oligomers of Abeta((25-35)) peptide but not to equine lysozyme amyloid or S100b protein in bulbectomized animals. The positive immunotropic effect of noopept to Abeta((25-35)) peptide prefibrillar aggregates was more marked in sham-operated compared to the bulbectomized subjects which were characterized by an overall suppression of immunoreactivity. Enhancement of the immune response to Abeta((25-35)) peptide prefibrils caused by noopept may attenuate the neurotoxic consequences of amyloid fibrillization and also be associated with an improvement in spatial memory in bulbectomized mice. These actions of noopept, combined with its previously reported neuroprotective and cholinomimetic properties, suggests that this dipeptide may well be useful for improving cognitive deficits induced by neurodegenerative diseases.

Alzheimer Disease↗

PubMed2004

[Influence of chronic epilepsy on spatial memory retrieval in rats].

OBJECTIVE: To investigate the influence of chronic epilepsy on spatial memory retrieval in rats, and to evaluate the effects of TAK-147, an acetylcholinesterase inhibitor, and histidine, the precursor of histamine, on the amnesia induced by epilepsy. METHODS: After successfully trained in the 8-arm (4-arm baited) radial maze, the rats were ip injected with a subconvulsive dose of pentylenetetrazole (PTZ) every 48 h until fully kindled. Memory retrieval was tested at the same maze. RESULT: Impairment of memory retrieval was in a steady state 1 to 18 days after fully kindled, the ability of memory retrieval returned to the control level 31 days after fully kindled. TAK-147 showed an ameliorating effect on memory impairment induced by epilepsy, including reference and working memory in a dose-dependent manner. Histidine only ameliorated reference but not working memory. CONCLUSION: PTZ-kindled seizure impair spatial memory retrieval, which it might be due to a decrease of brain acetylcholine and histamine induced by epilepsy.

Animals↗

PubMed1984

Effects of cholinergic and monoaminergic antagonists and tranquilizers upon spatial memory in rats.

To explore the pharmacological mechanisms of the spatial memory, performance on the radial arm maze was tested in rats under the following drugs, using a within-subject design; scopolamine (0.25 and 0.5 mg/kg), methylscopolamine (0.5 and 1 mg/kg), phentolamine (5 and 10 mg/kg), propranolol (10 and 20 mg/kg), chlorpromazine (1 and 2 mg/kg), and chlordiazepoxide (5 and 10 mg/kg). The number of correct choices was significantly decreased by scopolamine, while the other drugs, including methylscopolamine, showed no effects on the correct choices. Almost all drugs affected the running time. These findings indicate that the brain cholinergic system is involved in the spatial memory.

Animals↗

PubMed1995

Acute ethanol impairs spatial memory but not stimulus/response memory in the rat.

The present studies investigate how acutely administered ethanol (ETOH) affects the use of spatial memory. Previous electrophysiological results have shown that acutely administered ETOH alters the firing of hippocampal neurons and that prenatal or chronic exposure to ETOH produces deficits on spatial learning tasks, tasks dependent on the hippocampus. In contrast, it has also been demonstrated that acutely administered ETOH does not impair spatial localization. In the current studies, rats were trained to perform a spatial or stimulus/response task under saline. After training, rats were injected with ETOH, and the use of spatial or stimulus/response memory was tested. Acutely administered ETOH impaired the use of spatial memory, but not the use of stimulus/response memory. Because the use of spatial memory requires an intact hippocampus, the present studies suggest that acutely administered ETOH selectively impairs behaviors dependent on the hippocampus.

Animals↗

PubMed2005

Olanzapine attenuates the okadaic acid-induced spatial memory impairment and hippocampal cell death in rats.

It is hypothesized that olanzapine, an atypical antipsychotic drug, has beneficial effects on cognitive impairment and neuropathological changes in treating neurodegenerative diseases. In the present study, we investigated the effects of chronic administration of olanzapine on the spatial memory impairment and hippocampal cell death induced by the direct injection of okadaic acid (OA), a potent neurotoxin, into the rat hippocampus. After being pretreated with olanzapine (0.5 or 2 mg/kg/day, i.p.) for 2 weeks, the rats were unilaterally microinjected with OA (100 ng) into the hippocampus, and then were continuously administrated with olanzapine for an additional week The rats were trained on a spatial memory task in an eight-arm radial maze before OA administration, and tested on the same task 18 h after the last olanzapine injection. After the behavioral test, the rats were killed for Nissl staining and terminal deoxynucleutidyl transferase-mediated biotinylated UTP nick end labeling staining. OA significantly induced spatial memory impairment, and caused pyramidal cell loss in the CAI and apoptotic cell death in the hippocampus. Olanzapine significantly attenuated OA-induced spatial memory impairment and the OA-induced neuropathological changes in the hippocampus. These findings suggest that olanzapine may have therapeutic effects in treatment of cognitive impairment and neuropathological changes of schizophrenia and other neurodegenerative diseases.

Analysis of Variance↗

PubMed1984

Persistence of spatial memory in the Morris water tank task.

Persistence of the spatial memory record was examined in 30 rats overtrained in the working memory version of the Morris water tank task. In Experiment 1, the animal had to find during the acquisition trial an invisible underwater platform randomly located at one of 4 possible sites in the pool. Retention test was performed 1 min, 60 min, 4 h or 24 h later with the same position of the platform and same or changed position of the start. Whereas in the acquisition trials the rats reached the goal after 12 s on average, the latency in the retrieval trials increased with the acquisition-retrieval interval. It was 5 s with the 1-min delay and exponentially approached, but did not quite reach the acquisition trial latency with the 24-h delay. In Experiment 2 the rats were started from the same position of the tank to goal positions changing from trial to trial in a prearranged sequence. There were either 1-h or alternating 1-min and 2-h intervals between the 6 daily trials. The latencies were long during the first trial and whenever the goal changed and short when the goal remained the same as on the previous trial. The latencies were not significantly influenced by intertrial interval in the 1 min to 2 h range. It is concluded that the decay of spatial memory in the water tank task is slow and is little affected by proactive interference.

Animals↗

PubMed2001

Ameliorative effect of vasopressin-(4-9) through vasopressin V(1A) receptor on scopolamine-induced impairments of rat spatial memory in the eight-arm radial maze.

In order to clarify the mechanism by which pGlu-Asn-Cys(Cys)-Pro-Arg-Gly-NH(2) (vasopressin-(4-9)), a major metabolite C-terminal fragment of [Arg(8)]-vasopressin (vasopressin-(1-9)), improves learning and memory, we used several different drugs such as an acetylcholine receptor antagonist, a Ca(2+)/calmodulin-dependent protein kinase II inhibitor, vasopressin receptor antagonists and L-type Ca(2+) channel blocker to disrupt spatial memory in rats. Moreover, we examined the effect of vasopressin-(4-9) on acetylcholine release in the ventral hippocampus using microdialysis. Vasopressin-(4-9) (10 fg/brain, i.c.v.) improved the impairment of spatial memory in the eight-arm radial maze induced by scopolamine, pirenzepine and Ca(2+)/calmodulin -dependent protein kinase II inhibitor. Pirenzepine, a vasopressin V(1A) receptor antagonist, and L-type Ca(2+) channel blocker, but not a vasopressin V(2) receptor antagonist, suppressed the effects of vasopressin-(4-9) on scopolamine-induced impairment of spatial memory. Moreover, vasopressin-(4-9) did not affect acetylcholine release in the ventral hippocampus of intact rats or of scopolamine-treated rats as assessed by microdialysis. These results suggest that vasopressin-(4-9) activates vasopressin V(1A) receptors on the postsynaptic membrane of cholinergic neurons, and induces a transient influx of intracellular Ca(2+) through L-type Ca(2+) channels to interact with muscarinic M(1) receptors. The activation of these processes by vasopressin-(4-9) is critically involved in the positive effect of vasopressin-(4-9) on scopolamine-induced impairment of spatial memory.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed2003

Post-ischemic administration [correction of administeration] but not pre-ischemic administration [correction of administeration] of NG-nitro-L-arginine prevents spatial memory impairments and apoptosis by an inhibition of a delayed increase in NOx- in the hippocampus following repeated cerebral ischemia.

In the present study, we investigated the effects of N(G)-nitro-L-arginine (L-NAME), an inhibitor of nitric oxide synthase, on repeated cerebral ischemia-induced impairment of spatial memory of the 8-arm radial maze in rats. Repeated ischemia (10 min ischemia x 2 times with 1 h interval) impaired the spatial memory in the 8-arm radial maze test and produced apoptosis in the hippocampus 7 days after final occlusion, and gradually increased the NO(x)(-) levels approximately 30-180 min after the second reperfusion. Post-ischemic administration of L-NAME at a dose of 50 mg/kg, i.p. 30 min following the second occlusion, significantly attenuated the repeated ischemia-induced impairment of spatial memory in the 8-arm radial maze test and suppressed apoptosis in the hippocampus, and also significantly suppressed a delayed increase in the NO(x)(-) levels induced by repeated ischemia. However, pre-ischemic administration of L-NAME at a dose of 50 mg/kg, i.p. 30 min before the first occlusion, caused about 90% mortality (the mortality rate of vehicle-treated group was 10%). These results suggest that the delayed generation of NO(x)(-) may cause spatial memory impairment and induction of apoptosis in the hippocampus in rats subjected to repeated ischemia.

Animals↗

PubMed1994

Hypobaric hypoxia impairs spatial memory in an elevation-dependent fashion.

The effects of various levels of hypobaric hypoxia, exposure to reduced atmospheric pressure, on spatial memory in rats were examined. Hypobaric hypoxia simulates high altitude conditions where substantial deficits in human cognitive performance occur. However, few studies have measured cognitive changes in animals during exposure to this type of hypoxia. Male Fischer 344 rats were tested in the learning set version of the Morris water maze, a test known to assess spatial memory. Rats were tested at 2 and 6 hours while exposed to a range of simulated altitudes: sea level, 5500 m, 5950 m, and 6400 m. Altitude exposures at 5950 or 6400 m decreased both reference and working memory performance, as demonstrated by latency, distance, and speed measures, in an elevation-dependent fashion. During sea level testing on the day following hypobaric exposure, decrements in reference memory were still observed on all dependent measures, but only speed was impaired on the working memory task. These results agree with human studies that demonstrate elevation-dependent impairments in spatial memory performance during exposure to hypobaric hypoxia. The deficits may be attributable to changes in hippocampal cholinergic function.

Altitude↗

PubMed1997

Steroid Hormone Modulation of Hippocampal Dependent Spatial Memory.

Recent studies show that the adult CNS is capable of considerable re-structuring and re-growth, a property previously thought limited to the developmental period. Hormones play an important role in many of these plastic processes, and the hippocampus, as a target for all the major classes of steroid hormones, undergoes considerable remodeling. Since it is critical for mediating tasks requiring spatial memory, the hippocampus can serve as an important model for understanding not only the mechanisms underlying plasticity of brain circuits but also how these changes impact on a higher order function, spatial memory. In this review, the effects of steroid hormones on hippocampal remodeling are discussed, and the ability of estradiol to enhance spatial memory as well as the ability of both excessive or diminished corticosteroid levels to impair spatial memory are described. The neural mechanisms for these effects, as well as previous and current contributions of McEwen and colleagues to this expanding area of research, are discussed.

Journal Article↗

PubMed2002

[Effects of TAK-147, a novel acetylcholinesterase inhibitor, on spatial memory deficit as evaluated by Morris water maze of rats]

OBJECTIVE: To evalute the effects of TAK-147, a novel acetylcholinesterase inhibitor on rat spatial memory deficit using the Morris water maze. METHODS: Morris water maze was used to measure spatial memory in rats, and open field test was used to analysis locomotor activity. RESULTS: Scopolamine (0.4mg/kg,IP) significantly increased the latency period in memory acquisition. Intraperitoneal TAK-147 injection ameliorated scopolamine-induced deficit in a dose-related manner. A significant effect was obtained at doses of 0.3 and 1.0 mg/kg. Both TAK-147 (0.3 and 1.0 mg/kg) and tacrine (3 and 5 mg/kg) significantly reversed scopolamine (1.5 mg/kg) increased latency in memory retrieval. However, TAK-147 had a more potent effect than tacrine. In the locomotor test, TAK-147 created no appreciable change, compared with scopolamine or saline. CONCLUSION: A novel acetycholinesterase inhibitor, TAK-147 ameliorates the scopolamine induced impaired spatial memory in rats.

Journal Article↗

PubMed1982

Role of retroactive interference in the spatial memory of normal rats and rats with hippocampal lesions.

The importance of retroactive interference (RI) in memory for spatial locations was studied by using a 12-arm radial maze and a standard RI paradigm. Animals in the RI condition first learned to choose 4 of the 12 arms, followed by training to a second set of 4 arms. In the control condition for interference, rats learned the first set of arms but were not trained to approach the second set. Thereafter, animals in each interference condition were assigned to groups (hippocampal, cortical control, unoperated control), the operations were carried out, and then all animals were tested for retention of the set of arms learned first. Contrary to predictions of the cognitive map theory, O'Keefe & Nadel, 1978), RI was found in control animals. The severe memory deficit found in hippocampals was not influenced by the interference variable. In addition to impaired performance early in relearning, rats with hippocampal lesions continued to make many errors throughout the 10 wk of testing, including choices to unbaited arms and repeated entries into baited arms. However, hippocampals eventually learned not to reenter unbaited arms. These data indicate a deficit in the selection and utilization of sets of responses and are interpreted as implicating the hippocampus in retrieval processes.

Animals↗