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PubMed2006

Effects of D-galactose on the expression of hippocampal peripheral-type benzodiazepine receptor and spatial memory performances in rats.

The changes in spatial memory performances and the binding of hippocampal peripheral-type benzodiazepine receptor (PBR) induced by D-galactose (D-gal) were investigated in rats. The animals were randomly divided into two groups: saline-treated group and D-gal-induced aging group. All rats received 56 days of injection followed by 5 days of behavioral tests. The D-gal-induced aging rats presented significant impairment in water maze performance, compared with that in the saline-treated rats. A significant decrease in [3H]PK11195 binding in the synaptosomes from hippocampus in the D-gal-induced aging rats was observed, compared to that in the saline-treated rats. Meanwhile, the Scatchard analysis revealed that there was a decrease in Bmax, with no significant change in KD. Further analysis demonstrated that water maze performance was closely related to the PK11195 binding in all rats. These results suggest that D-gal decreased the density of PBR in hippocampal synaptosomes, which may be attributable to the progressive pathogenesis of aging in rats.

Aging↗
PubMed2004

Long-term spatial memory: introduction and guide to the special section.

This article provides an introduction to the Special Section on Long-Term Spatial Memory in the journal Neuropsychology. It defines long-term spatial memory, explores how it has been considered historically, and provides brief descriptions of the principle cognitive mechanisms, with a guide to the terminology used in this field.

Animals↗
PubMed2003

Long-term moderate elevation of corticosterone facilitates avian food-caching behaviour and enhances spatial memory.

It is widely assumed that chronic stress and corresponding chronic elevations of glucocorticoid levels have deleterious effects on animals' brain functions such as learning and memory. Some animals, however, appear to maintain moderately elevated levels of glucocorticoids over long periods of time under natural energetically demanding conditions, and it is not clear whether such chronic but moderate elevations may be adaptive. I implanted wild-caught food-caching mountain chickadees (Poecile gambeli), which rely at least in part on spatial memory to find their caches, with 90-day continuous time-release corticosterone pellets designed to approximately double the baseline corticosterone levels. Corticosterone-implanted birds cached and consumed significantly more food and showed more efficient cache recovery and superior spatial memory performance compared with placebo-implanted birds. Thus, contrary to prevailing assumptions, long-term moderate elevations of corticosterone appear to enhance spatial memory in food-caching mountain chickadees. These results suggest that moderate chronic elevation of corticosterone may serve as an adaptation to unpredictable environments by facilitating feeding and food-caching behaviour and by improving cache-retrieval efficiency in food-caching birds.

Adaptation, Physiological↗
PubMed2002

Impairment of long-term potentiation and spatial memory in leptin receptor-deficient rodents.

Leptin is well known to be involved in the control of feeding, reproduction and neuroendocrine functions through its action on the hypothalamus. However, leptin receptors are found in brain regions other than the hypothalamus (including the hippocampus and cerebral cortex) suggesting extrahypothalamic functions. We investigated hippocampal long-term potentiation (LTP) and long-term depression (LTD), and the spatial-memory function in two leptin receptor-deficient rodents (Zucker rats and db/db mice). In brain slices, the CA1 hippocampal region of both strains showed impairments of LTP and LTD; leptin (10(-12) M) did not improve these impairments in either strain. These strains also showed lower basal levels of Ca(2+)/calmodulin-dependent protein kinase II activity in the CA1 region than the respective controls, and the levels did not respond to tetanic stimulation. These strains also showed impaired spatial memory in the Morris water-maze test (i.e. longer swim-path lengths during training sessions and less frequent crossings of the platform's original location in the probe test. From these results we suggest that the leptin receptor-deficient animals show impaired LTP in CA1 and poor spatial memory due, at least in part, to a deficiency in leptin receptors in the hippocampus.

Animals↗
PubMedDate not supplied

Exercise does not modify spatial memory, brain autoimmunity, or antibody response in aged F-344 rats.

Old F-344 rats were given endurance training over a 10-week period on a motorized treadmill. This treatment resulted in substantial heart-to-body weight ratio increases, indicative of effective training. To determine whether endurance training might alter some of the known immune system and cognitive changes observed during aging, exercised old rats were compared to nonexercised old and young controls on three variables: in vivo antigen-specific immune activity, brain-reactive antibody formation, and spatial memory. The exercise training did not influence any of these measures in the old rats. Both groups of old rats showed poorer antibody response to a specific antigen, more brain-reactive antibody formation, and poorer spatial memory than the young controls. There was, however, a significant relationship between brain-reactive antibody formation and spatial memory performance, regardless of training condition.

Aging↗
PubMed1998

Moderate, long-term, alcohol consumption potentiates normal, age-related spatial memory deficits in rats.

A modified "Samson" sucrose fading procedure was used to establish voluntary consumption of a 20% ethanol (EtOH) solution in male Sprague-Dawley rats for 18 consecutive months. Intakes were stable over the life span, and corresponded to the moderate to high levels of intake typically observed in human "social" drinkers and alcoholics. The Morris Water Maze (WM), Olton Radial Arm Maze (RM), and a "balance beam" test were used to assess the effects of alcohol and aging on spatial memory and motor function. Aged EtOH-consuming rats (AGED/ALC) demonstrated impaired task acquisition, relative to aged controls (AGED), not reaching criterion performance in either spatial memory task even when given four additional days of training. AGED/ALC rats scored significantly lower on percent correct out of the first eight arm entries, and committed more perseverative errors in the RM. There were no significant performance differences between AGED and AGED/ALC rats on a balance beam test of fine motor coordination and equilibrium, suggesting that deficits observed in the RM and WM were not related to differential motor functioning. These results demonstrated that long-term, moderate, oral self-administration of EtOH, within the range typically consumed by humans, had adverse effects on spatial memory in rats, and that such a pattern of EtOH consumption seemed to exacerbate the decline in cognitive functioning associated with normal aging.

Aging↗
PubMed1988

Spatial memory impairment and central muscarinic receptor loss following prolonged treatment with organophosphates.

Memory impairment is one of the recurrent complaints of agricultural workers repeatedly exposed to organophosphorus insecticides. In an effort to establish an animal model for such behavioral effects, which would allow studying its underlying biochemical mechanism(s), in this study we evaluated spatial memory in animals following repeated organophosphate exposure. Male Long-Evans rats were given daily i.p. injections of either diisopropylfluorophosphate (DFP; 1 mg/kg/day) or disulfoton (O,O-diethyl S-[2-(ethylthio)ethyl] phosphorodithioate; 2 mg/kg/day) for 14 days. Acetylcholinesterase activity was inhibited 71-77% in the cortex, hippocampus, and striatum of rats treated with DFP, and 73-74% in those treated with disulfoton. Binding of [3H]quinuclidinyl benzilate ([3H]QNB) to cholinergic muscarinic receptors in the same brain areas was reduced 16-28% in organophosphate-treated rats. This decrease was due to a reduction in muscarinic receptor density (Bmax) with no changes in receptor affinity. At the end of the treatment rats were tested for spatial memory using the spontaneous alternation task in a T-maze. Rates of true spontaneous alternation were 64.4, 45.0, and 44.8% in animals which received corn oil, DFP, or disulfoton, respectively (P less than 0.05). These results indicate that prolonged inhibition of acetylcholinesterase caused by repeated organophosphate exposure alters spatial memory functions in rats, as well as causing a loss of muscarinic receptors. Considering the role of the cholinergic system in cognitive processes, these biochemical alterations could be related to the observed behavioral changes and may offer a potential explanation of the memory impairment reported by workers chronically exposed to organophosphates.

Acetylcholinesterase↗
PubMed2001

Effect of H1-antagonists on spatial memory deficit evaluated by 8-arm radial maze in rats.

AIM: To evaluate effects of certain H1-antagonists on spatial memory with 8-arm radial maze performance of rats. METHODS: Eight-arm radial maze performance was used to measure spatial memory in rats. RESULTS: Chronic treatments of classical H1-antagonists, diphenhydramine (5 mg/kg) and pyrilamine (20 mg/kg) impaired acquisition memory process regarding both parameters of radial maze performance. In addition, the memory retrieval process was also impaired significantly by a single administration of diphenhydramine (5, 10 mg/kg) and pyrilamine (50 mg/kg). However, the newly developed H1-antagonist, epinastine caused no appreciable effect on both acquisition and retrieval memory even at a high dose of 50 mg/kg. The memory deficit induced by diphenhydramine (10 mg/kg) or pyrilamine (50 mg/kg) was reversed by tacrine (1 mg/kg). CONCLUSION: Histamine H(1)-receptors plays a certain role in spatial cognition, and its action may be due to both histaminergic and cholinergic neurons.

Animals↗
PubMed2006

The cognitive neuroscience of remote episodic, semantic and spatial memory.

The processes and mechanisms implicated in retention and retrieval of memories as they age is an enduring problem in cognitive neuroscience. Research from lesion and functional neuroimaging studies on remote episodic, semantic and spatial memory in humans is crucial for evaluating three theories of hippocampal and/or medial temporal lobe-neocortical interaction in memory retention and retrieval: cognitive map theory, standard consolidation theory and multiple trace theory. Each theory makes different predictions regarding first, the severity and extent of retrograde amnesia following lesions to some or all of the structures mentioned; second, the extent of activation of these structures to retrieval of memory across time; and third, the type of memory being retrieved. Each of these theories has strengths and weaknesses, and there are various unresolved issues. We propose a unified account based on multiple trace theory. This theory states that the hippocampus is needed for re-experiencing detailed episodic and spatial memories no matter how old they are, and that it contributes to the formation and assimilation of semantic memories and schematic spatial maps.

Amnesia, Retrograde↗
PubMed2002

A role of Fos expression in the CA3 region of the hippocampus in spatial memory formation in rats.

Activity-dependent plastic changes in the strength of synaptic connections are considered to underlie learning and memory. Activation of neurons by a variety of stimuli influences the level of expression of the immediate-early gene c-fos, and the heterodimer of the gene product, Fos, regulates transcription of other genes. Therefore, Fos is regarded as a mediator by which brief stimuli trigger long-term changes in the synaptic connections. Here we show that Fos expression in the CA3 region of the hippocampus may be obligatory for spatial memory formation in a radial arm maze test. Fos-positive cells increased in the cerebral cortices and the CA3 region of the dorsal hippocampus during the course of radial arm maze training in rats. Inhibition of Fos expression in this region of the hippocampus, but not the cingulate and motor cortex, by means of antisense oligonucleotide treatment resulted in an impairment of spatial memory formation. Our results support the hypothesis that the inducible transcription factor c-fos is essential for encoding spatial memory.

Animals↗
PubMed2006

Berberine chloride can ameliorate the spatial memory impairment and increase the expression of interleukin-1beta and inducible nitric oxide synthase in the rat model of Alzheimer's disease.

BACKGROUND: Berberine is the major alkaloidal component of Rhizoma coptidis, and has multiple pharmacological effects including inhibiting acetylcholinesterase, reducing cholesterol and glucose, lowering mortality in patients with chronic congestive heart failure and anti-inflammation etc. Thus berberine is a promising drug for diabetes, hyperlipemia, coronary artery disease and ischemic stroke etc. The present study was carried out to investigate the effect of berberine chloride on the spatial memory, inflammation factors interleukin-1 beta (IL-1beta) and inducible nitric oxide synthase (iNOS) expression in the rat model of Alzheimer's disease (AD) which was established by injecting Abeta (1-40) (5 microgram) into the rats hippocampuses bilaterally. RESULTS: The rats were given berberine chloride (50 mg/kg) by intragastric administration once daily for 14 days. The spatial memory was assayed by Morris water maze test, IL-1beta and iNOS in the hippocampus were assayed by immunohistochemistry and real time polymerase chain reaction (PCR). Intragastric administration of berberine significantly ameliorated the spatial memory impairment and increased the expression of IL-1beta, iNOS in the rat model of AD. CONCLUSION: Berberine might be beneficial to AD by intragastric administration though it might exaggerate the inflammation reaction.

Alzheimer Disease↗
PubMed1987

Single unit activity in the rat hippocampus during a spatial memory task.

Single unit activity was recorded from complex spike cells in the hippocampus of the rat while the animal was performing a spatial memory task. The task required the animal to choose the correct arm of a 4 arm plus-shaped maze in order to obtain reward. The location of the goal arm was varied from trial to trial and was identified by 6 controlled spatial cues which were distributed around the enclosure and which were rotated in step with the goal. On some trials these spatial cues were present throughout the trial (spatial reference memory trials) while on other trials they were present during the first part of the trial but were removed before the rat was allowed to choose the goal (spatial working memory trials). On these latter trials the animal had to remember the location of the cues and/or goal during the delay in order to choose correctly. 55 units were recorded during sufficient reference memory trials for the relationship between their firing pattern and different spatial aspects of the environment to be determined. 33 units had fields with significant relations to the controlled cues while 16 had significant relations to the static background cues, those cues in the environment which did not change position from trial to trial. Of 43 units which could be tested for their relation to the shape of the maze arms themselves, 15 showed such a relationship. Therefore the place units can be influenced by different aspects of the spatial environment but those related to the task requirement appear to be more potent. Interaction effects between the different spatial factors also influenced the firing pattern of some units. Of particular interest was the interaction between the controlled cues and the static background cues found in some cells since this might shed some light on how the hippocampus enables the rat to solve the memory task. 30 units with place fields related to the controlled cues were recorded during successful performance on spatial working memory trials as well as during spatial reference memory trials. The place fields of 90% of these units were maintained during the retention phase of the memory trials. During the recording of some units, other types of trial were given as well. On control trials, the cues were removed before the rat was placed on the maze. These trials provided controls for the potential influence of information left behind by the controlled cues and for the influence of the animal's behaviour on the unit activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1977

Spatial memory and hemispheric locus of lesion.

Corsi's cube test was given to 40 control and 80 brain-damaged patients to assess the relation of different aspects of spatial memory to the hemispheric locus of lesion. Spatial span was found affected by injury producing visual field defect (VFD), regardless of the side of the lesion. Delayed reproduction of a 3 cube sequence (which was within the span of every patient) was performed more poorly by patients with right hemisphere damage and VFD than by controls. This was true whether the delay was unfilled or filled with a counting activity, the two conditions being equally effective in bringing about the inferiority of the right brain-damaged group. Learning to criterion up to a maximum of 50 trails a supraspan sequence was failed by 65% of right brain-damaged patients with VFD, a percentage significantly higher than that found not only in the control group, but also in any other brain-damaged group. These findings point to the dominant role played by the posterior region of the right hemisphere in subserving spatial memory mechanisms, especially when the acquisition of stable traces is requested.

Brain Damage, Chronic↗
PubMed1979

Spatial memory deficit following fimbria-fornix lesions: independent of time for stimulus processing.

The present experiment examined the possible role of stimulus processing time in the spatial memory deficit found following fimbria-fornix lesions in rats. Rats were trained preoperatively on a radial arm maze in a procedure that placed them at the end of each arm and confined them there for 30 seconds. This confinement period was markedly longer than the few seconds the rats normally spend there in the usual test procedure. Rats with fimbria-fornix lesions performed no better than expected by chance on the first choice after placements. Although performance on subsequent choices was above chance, this was due to a strong turning pattern; when this pattern was interrupted, performance was no greater than that expected by chance on all choices. These data demonstrate that the deficit in the radial arm maze resulted primarily from a difficulty in spatial memory, rather than from an insufficient time for processing stimulus information.

Animals↗
PubMed2000

Facilitating effects of histamine on spatial memory deficit induced by scopolamine in rats.

AIM: To investigate whether or not histamine was involved in scopolamine-induced spatial memory deficits evaluated in 8-arm radial maze performance of 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 histamine (100 or 200 ng) or thioperamide (50 micrograms), and intraperitoneal (i.p.) injection of histidine (1000 mg/kg) ameliorated memory impairment induced by scopolamine regarding both parameters of radial maze performance. 2-Thiazolylethylamine, but not 4-methylhistamine showed the similar effect to histamine. Both histamine (200 ng, icv) and histidine (1000 mg/kg, i.p.) were equally effective in increasing the histamine content in the cortex, hippocampus, and hypothalamus. CONCLUSION: These results suggest that brain histamine plays an important role in learning and memory, and its action may be due to cholinergic neurons.

Animals↗
PubMed2006

Chronic stress impairs spatial memory and motivation for reward without disrupting motor ability and motivation to explore.

This study uses an operant, behavioral model to assess the daily changes in the decay rate of short-term memory, motivation, and motor ability in rats exposed to chronic restraint. Restraint decreased reward-related motivation by 50% without altering memory decay rate or motor ability. Moreover, chronic restraint impaired hippocampal-dependent spatial memory on the Y maze (4-hr delay) and produced CA3 dendritic retraction without altering hippocampal-independent maze navigation (1-min delay) or locomotion. Thus, mechanisms underlying motivation for food reward differ from those underlying Y maze exploration, and neurobiological substrates of spatial memory, such as the hippocampus, differ from those that underlie short-term memory. Chronic restraint produces functional, neuromorphological, and physiological alterations that parallel symptoms of depression in humans.

Adrenal Glands↗
PubMed2003

Antisense hippocampal knockdown of NMDA-NR1 by HVJ-liposome vector induces deficit of prepulse inhibition but not of spatial memory.

Considerable evidence suggests that an N-methyl-D-aspartate (NMDA) receptor plays a crucial role in memory and cognitive function. To identify the role of this receptor in higher functions of the brain, we delivered antisense oligonucleotides against an NMDA-NR1 subunit (NR1) to the hippocampus in rats using the HVJ-liposome-mediated gene-transfer method. NR1 hippocampal knockdown was performed by the focal injection of the NR1 antisense-HVJ-liposome complex into the bilateral hippocampus. The blocking effect of NR1-antisense on the expression of NR1 was confirmed by Western blot analysis. Spatial memory was tested by a water maze task, and sensorimotor gating was examined by prepulse inhibition (PPI). Western blot analysis demonstrated that the NR1-antisense treatment specifically provided the down-regulation (about 30%) of NR1 protein levels in the hippocampus. The water maze task showed that the antisense treatment did not affect spatial memory, while the PPI test revealed that NR1 hippocampal knockdown caused a deficit in sensorimotor gating. We conclude that mild dysfunction of hippocampal NMDA receptor causes sensorimotor gating deficit and relatively intact in spatial memory.

Animals↗