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PubMed2001

Language, space, and the development of cognitive flexibility in humans: the case of two spatial memory tasks.

Prior experiments have shown that young children, like adult rats, rely mainly on information about the macroscopic shape of the environment to reorient themselves, whereas human adults rely more flexibly on combinations of spatial and non-spatial landmark information. Adult rats have also been shown to exhibit a striking limitation in another spatial memory task, movable object search, again a limitation not shown by human adults. The present experiments explored the developmental change in humans leading to more flexible, human adult-like performance on these two tasks. Experiment 1 identified the age range of 5-7 years as the time the developmental change for reorientation occurs. Experiment 2 employed a multiple regression approach to determine that among several candidate measures, only a specific language production measure, the production of phrases specifying exactly the information needed to solve the task like adults, correlated with the reorientation performance of children in this age range. Experiment 3 revealed that similar language production abilities were associated with more flexible moving object search task performance. These results, in combination with findings with human adults, suggest that language production skills play a causal role in allowing older humans to construct novel representations rapidly, which can then be used to transcend the limits of phylogenetically older cognitive processes.

Adult↗

PubMed2006

Impairments in spatial memory retention of GFAP-apoE4 female mice.

The human apolipoprotein E isoforms, apoE2, apoE3, and apoE4, have differential effects on brain function. Compared to apoE3, apoE4 increases the risk of age-related cognitive decline in humans and female mice expressing apoE in neurons. Here, we show impaired spatial memory retention in female mice expressing apoE4 in astrocytes compared to those expressing apoE3 in astrocytes or lacking apoE. Thus, apoE4 impairs cognition whether expressed in neurons or astrocytes.

Analysis of Variance↗

PubMed2002

Early spatial memory deficit induced by 2,5-hexanedione in the rat.

2,5-Hexanedione (2,5-HD), the major common neurotoxic metabolite of n-hexane and methyl n-butyl ketone, causes a delayed neuropathy with associated sensorimotor impairments. The question arises as to whether specific cognitive deficits occur even prior to changes in sensorimotor ability. The present experiments examined the effects of 2,5-HD on spatial navigation of rats in a water maze at levels/times that did not affect spontaneous exploratory motor activity in an open field holeboard apparatus. Exposure to 1% 2,5-HD in the drinking water for 2 weeks did not significantly affect escape learning, as measured by latency to find a hidden platform. However, 2,5-HD treated animals were impaired in the use of a spatial strategy during a recall test. A similar impairment in spatial memory was observed after i.p. injection of 500 mg/kg/day 2,5-HD for 4 days, in the absence of significant changes in sensorimotor ability or weight loss. Thus 2,5-HD may mediate some of the cognitive effects of hexacarbons and these changes can occur prior to the development of motor symptoms.

Animals↗

PubMed1989

Brain transplants enhance rather than reduce the impairment of spatial memory and olfaction in bulbectomized rats.

The possibility to compensate the loss of olfactory and non-olfactory functions due to removal of the olfactory bulb by embryonal brain grafts was investigated in adult rats. Spatial working memory was examined in an 8-arm radial water maze task 6 weeks after bulbectomy. During 15 daily trials, performance gradually improved in bulbectomized controls (n = 10) and in rats with olfactory bulb transplants (n = 9), but did not attain that of intact controls (n = 10). No improvement was observed in the rats with substantia nigra grafts (n = 8). Eleven weeks after bulbectomy, the same rats were tested in the water tank navigation task. The performance improved during ten 12-trial sessions in bulbectomized rats less than in intact controls, but more than in the transplanted rats. The olfactory food retrieval test performed 14 weeks after bulbectomy revealed almost full recovery of smell in bulbectomized rats, but not in the transplanted animals. It is concluded that the spatial memory deficit is probably due to bulbectomy-induced interference with septohippocampal function which is not alleviated, but rather enhanced by transplantation. The results suggest that the effect of brain grafting is not always beneficial.

Animals↗

PubMed2000

BDNF protects against spatial memory deficits following neonatal hypoxia-ischemia.

Hypoxic-ischemic (H-I) brain injury in the human perinatal period often leads to significant long-term neurobehavioral dysfunction in the cognitive and sensory-motor domains. Using a neonatal H-I injury model (unilateral carotid ligation followed by hypoxia) in postnatal day seven rats, previous studies have shown that neurotrophins, such as brain-derived neurotrophic factor (BDNF), can be protective against neural tissue loss. The present study explored potential relationships between neural protective and behavioral protective strategies in this neonatal H-I model by determining if neonatal H-I was associated with behavioral spatial learning and memory deficits and whether the neurotrophin BDNF was protective against both brain injury and spatial learning/memory dysfunction. Postnatal day seven rats received vehicle or BDNF pretreatments (intracerebroventricular injections) followed by H-I or sham treatments and then tested for spatial learning and memory on the simple place task in the Morris water maze from postnatal days 20 to 30, and their brains were histologically analyzed at 4 weeks following treatments. H-I rats with vehicle pretreatment displayed significant tissue loss in the hippocampus (including CA1 neurons), cortex, and striatum, as well as severe spatial memory deficits (e.g., short probe times). BDNF pretreatment resulted in significant protection against both H-I-induced brain tissue losses and spatial memory impairments. These findings indicate that unilateral H-I brain injury in a neonatal rodent model is associated with cognitive deficits, and that BDNF pretreatment is protective against both brain injury and spatial memory impairment.

Animals↗

PubMed2006

A new test for long-term spatial memory using an operant chamber in mice.

As part of ongoing efforts to develop fully automated and standardized behavioral tasks to probe cognitive and mnemonic capabilities of mice, we have constructed a new rectangular operant chamber. The chamber contains numerous nose poke holes, distributed over three of its inner walls that are identifiable by their spatial locations. Using this apparatus, we have developed a 'spatial' memory task using a successive reversal discrimination paradigm. Mice learn to discriminate, by trial and error, the position of a single valid hole during a Presentation session wherein they obtained a maximum of 20 reinforcements or 15 min time elapsed. Following a delay interval, they were resubmitted to the same task (Test) using the same reinforced hole. Results indicated that C57BL/6 mice exhibited a significant improvement during the Test, the magnitude of the improvement (memory savings) being dependent on the length of retention intervals ranging from 5 min to 24h. In addition, discrimination performance was sensitive to scopolamine in a dose dependent manner. The simplicity in task set up and the minimal labor and space requirements make this task suitable for high throughput behavioral characterization of genetically modified mice.

Analysis of Variance↗

PubMed2000

Adrenergic activation of the nucleus tractus solitarius potentiates amygdala norepinephrine release and enhances retention performance in emotionally arousing and spatial memory tasks.

It is well documented that noradrenergic systems in the amygdala modulate memory formation, however, less research has examined how sources of limbic norepinephrine contribute to this process. The amygdala receives a dense supply of norepinephrine from neurons in the nucleus of the solitary tract (NTS). The present experiments examined whether adrenergic activation of these NTS neurons affects memory in learning tasks that are sensitive to amygdala norepinephrine release. Separate groups of male Sprague-Dawley rats were trained in either an emotionally arousing or spatial memory task. They then received vehicle or the adrenergic agonist epinephrine (50, 125, or 250 ng/0.5 microl) into the NTS. Rats given the 125 ng dose had significantly longer retention latencies on a 48 h inhibitory avoidance retention test and made a significantly higher percentage of correct responses on an 18 h delayed radial maze retention test. A third experiment using in vivo microdialysis and high performance liquid chromatography (HPLC) demonstrated that intra-NTS infusion of a memory-enhancing dose of epinephrine potentiated amygdala norepinephrine release. Collectively, these results suggest that stimulation of the NTS contributes to memory processing by influencing noradrenergic systems in the amygdala.

Adrenergic Agonists↗

PubMed1982

Spatial memory in older adults: effects of intentionality.

College students and elderly adults were presented with drawings for study that were placed on the left or right side of a photographic slide. Persons in the items-only condition studied only the target drawings, whereas persons in the items-position condition studied both the target drawing and its location to determine whether intentionality affected picture recognition or position recall. Half of the drawings were presented with an irrelevant adjacent drawing to assess the effect of presenting the target item relative to another drawing. The principal finding was that, although special memory was well above chance, the Hasher and Zack's criteria for automatic processing of this dimension were not met. Specifically, an age-related decline in spatial memory was observed, and intentionality to learn position affected item recognition and position recall. It was also found that older persons' memory for position was enhanced by the irrelevant drawings. Results are discussed primarily in terms of the Hasher and Zacks model of automatic processing and possible encoding strategies utilized by the elderly.

Adult↗

PubMed2006

Beyond spatial memory: the anterior thalamus and memory for the temporal order of a sequence of odor cues.

Influential recent proposals state that the anterior thalamic (AT) nuclei constitute key components of an "extended hippocampal system." This idea is, however, based on lesion studies that used spatial memory tasks and there has been no evidence that AT lesions cause deficits in any hippocampal-dependent nonspatial tasks. The present study investigated the role of the AT nuclei in nonspatial memory for a sequence of events based on the temporal order of a list of odors, because this task has recently been shown to depend on the integrity of the hippocampal formation. After preoperative training, rats with excitotoxic lesions of the AT nuclei showed a severe and selective postoperative impairment when required to remember the order of pseudorandom sequences of six odors. The rats with AT lesions were able instead to learn two new tasks that required recognition memory and the identification of the prior occurrence of events independent of their order. These results strongly matched those described after hippocampal lesions and provide the first unequivocal evidence of a detrimental effect of an AT lesion on a nonspatial hippocampal-dependent memory task.

Animals↗

PubMedDate not supplied

[Disruption of spatial memory in mice exposed to agroclavine].

The results of the study of the mnemotropic activity of the ergot alkaloid agroclavine are presented. Effects of this substance administered in doses of 1, 10, 25, 50, and 200 micrograms/kg on learning and spatial memory were studied in a Morris water maze. Agroclavine had no effect on learning but sharply impaired the retention. This memory impairment persisted for 48 h after the agroclavine administration. Agroclavine treatment did not affect the ability of mice to learn and retain a new skill. Possible mechanisms of the agroclavine effect on memory are discussed.

Animals↗

PubMed2000

Spatial memory averaging, the landmark attraction effect, and representational gravity.

The effect of a large stationary landmark on memory for the location of a stationary target was examined. Memory for a stationary target was displaced toward the landmark, and targets that were larger, further from, or above the landmark exhibited greater magnitudes of displacement. Displacement was generally larger when the landmark vanished prior to judgment than when the landmark was visible during judgment. Memory for stationary targets offset from the major vertical or horizontal cardinal axis of the landmark was also displaced toward that cardinal axis. The data support the hypotheses that spatial memory averaging of the locations of a target and landmark occurs, and that this averaging may be combined with representational gravity in determining the remembered position of a stationary target.

Humans↗

PubMed2006

Potentiation of ethanol in spatial memory deficits induced by some benzodiazepines.

Triazolam caused no significant increase in the total error at 0.05 and 0.1 mg/kg. However, at 0.2 mg/kg, it caused a significant increase in total error. Almost the same findings were observed with brotizolam and rilmazafone. That is, at 0.2 and 0.5 mg/kg of brotizolam, 0.5 and 1.0 mg/kg of rilmazafone caused no significant increase in the total error. However, brotizolam at 1.0 mg/kg and rilmazafone at 2.0 mg/kg caused a significant increase in total error. Triazolam (0.05 mg/kg) and ethanol (1.0 g/kg) showed no significant effect on the numbers of errors when used alone separately, but the simultaneous use of triazolam and ethanol caused a significant increase in total error. Almost the same findings were observed with the coadministration of brotizolam (0.2 mg/kg) or rilmazafone (0.5 mg/kg) with ethanol. These results clearly indicate that all the short-acting benzodiazepines used in the study showed potentiation by ethanol in spatial memory deficits in mice.

Animals↗

PubMed1981

Spatial memory following damage to hippocampal CA3 pyramidal cells with kainic acid: impairment and recovery with preoperative training.

The behavioral function of an intrinsic component of the hippocampus was investigated. Neurotoxic lesions of the CA3 region of the hippocampus impaired performance of a spatial memory task, and produced both hyperactivity and hyperreactivity to sensory stimulation. Both the magnitude and duration of these behavioral alterations depended on the amount of preoperative training received, and on the extent and locus of the lesion within the CA3 subfield. This study indicates that the CA3 subfield contributes to the performance of aat least three behavioral functions known to be mediated by the hippocampus. In addition, the lack of enduring deficits in the behavioral tests in which preoperative training was received suggests that, after loss of the CA3 subfield, some mechanism for recovery of function occurs within the hippocampus.

Animals↗

PubMed1992

Involvement of glycine site associated with the NMDA receptor in hippocampal long-term potentiation and acquisition of spatial memory in rats.

The effects of 7-chlorokynurenic acid (7-Cl-Kyn), a selective antagonist at the glycine site associated with the N-methyl-D-aspartate (NMDA) receptor, on hippocampal long-term potentiation (LTP) and behavioral performances in a spatial learning task were investigated. Extracellular recordings of evoked potential (population spike) were made in rat hippocampal slices. Perfusion of 7-Cl-Kyn (10(-5) M) inhibited the induction of LTP following a tetanic stimulation (51 or 101 pulses at 100 Hz) both in the Schaffer/commissural-CA1 pyramidal cell synapses and in the perforant path-dentate granule cell synapses. Acquisition of a spatial memory in the Morris water maze was examined using rats chronically cannulated for application of drugs. The intact and vehicle-injected rats learned easily to escape onto a hidden platform with short latencies, while the rats given an injection of 7-Cl-Kyn (10(-8) mol/brain, i.c.v.) prior to every session took a longer time and a longer path to escape even after all 5 sessions of trials. Injection of 7-Cl-Kyn did not affect the swimming speed, an index of swimming ability. This is the first report providing direct evidence that endogenous glycine supports the processes of learning and memory.

Animals↗

PubMed2005

The effects of regular aerobic exercise in adolescent period on hippocampal neuron density, apoptosis and spatial memory.

It is known that positive effects of regular aerobic exercise on cognitive functions in humans and also animals; but how to the effects of aerobic exercise in adolescent period is unknown. The present study examined the effects of regular aerobic exercise on spatial memory using the Morris water maze, cell density and apoptosis of hippocampus in adolescent rats. Twenty-two days of age male rats were run on a treadmill for 30 min/session at a speed of 8m/min and 0 degrees slope, five times a week for 8 weeks. The present study showed that exercise induced significant cognitive improvement throughout brain maturation in rats. The number of hippocampal CA1 and CA3 neurons, and gyrus dentatus neurons were significantly increased in the exercised rats. There was no significant difference of CA2 neuron density between exercise and control groups. There was no significantly differences in any groups according to the results of apoptosis that account of TUNEL positive cells. The present results suggest that regular moderate aerobic treadmill exercise benefit in cognitive functions. This result may derive from treadmill exercise-induced increase cell density without altering of apoptosis in the hippocampus and dentate gyrus of adolescent rats.

Animals↗

PubMedDate not supplied

Long-term treatment with estrogen and progesterone enhances acquisition of a spatial memory task by ovariectomized aged rats.

Female Sprague-Dawley rats were ovariectomized at 13 months of age. Four groups received different regimens of estrogen or estrogen plus progesterone replacement beginning either immediately, 3 months, or 10 months after ovariectomy and were compared with non-hormone-treated controls. Eight to twelve months after ovariectomy, animals were trained on a delayed matching-to-position (DMP) spatial memory task. Long-term treatment with estrogen or estrogen plus progesterone significantly enhanced acquisition of the DMP task by aged animals after long-term loss of ovarian function. Weekly administration of estrogen and progesterone was at least as effective as, if not more effective than, continuous treatment with estrogen alone. In addition, treatment initiated 3 months, but not 10 months, after ovariectomy was as effective at enhancing DMP acquisition as continuous estrogen treatment initiated immediately after ovariectomy, suggesting a window of opportunity after the loss of ovarian function during which hormone replacement can effectively prevent the effects of aging and hormone deprivation on cognitive function. These findings suggest that repeated treatment with estrogen and progesterone initiated within a specific period of time after the loss of ovarian function may be effective at preventing specific negative effects of hormone deprivation on brain aging and cognitive decline.

Aging↗

PubMed1997

Spatial memory deficits in patients with unilateral damage to the right hippocampal formation.

Patients with unilateral temporal lobe damage resulting from intractable temporal lobe epilepsy (TLE, n = 30) or from temporal lobe resection (temporal lobectomy, TLR, n = 47) were investigated on the Nine-box Maze. The task, analogous to the radial arm maze, was designed to compare spatial mapping and working memory theories of the functions of the hippocampus. The task provides measures of spatial, object, working and reference memory, incorporated into a within subjects design. The spatial component was designed to encourage the formation of allocentric rather than egocentric spatial representations. Spatial memory deficits were found (across working and reference memory components) in both TLE and TLR patients with right temporal lobe damage, with intact spatial memory in patients with corresponding left temporal lobe damage. Performance on the matched non-spatial (object) working memory component was equal to healthy controls for all groups. However all patient groups showed a deficit on object reference memory. These findings are discussed in relation to the underlying temporal lobe pathology and particularly atrophy of the hippocampal formation. Overall, the results support the cognitive mapping theory of hippocampal function, with the demonstration of a selective (and probably allocentric) spatial memory deficit in patients with right hippocampal damage.

Adolescent↗

PubMed2004

Protective effect of the alpha2-adrenoceptor antagonist, dexefaroxan, against spatial memory deficit induced by cortical devascularization in the adult rat.

The alpha2-adrenoceptor antagonist, dexefaroxan, has been shown in the rat to have neuroprotective and plastic effects against degenerative structural changes in elements of the basalocortical cholinergic system that result from cortical devascularization [Neuroscience 115 (2002) 41]. The present study, using the same experimental protocol, examined the functional consequences of cortical devascularization and dexefaroxan treatment in the Morris water maze memory test. Rats were first trained to find the hidden platform in the test, and then subjected to the devascularization procedure. Thirty-one days later, lesioned rats exhibited a significant deficit in recalling the platform location, compared with sham control animals. A 28-day subcutaneous infusion with dexefaroxan (0.63, 2.5, and 10 mg rat(-1) day(-1)), starting from the moment of the devascularization, protected against this spatial memory deficit.

Adrenergic alpha-2 Receptor Antagonists↗