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PubMed2002

Human hippocampus and viewpoint dependence in spatial memory.

Virtual reality was used to sequentially present objects within a town square and to test recognition of object locations from the same viewpoint as presentation, or from a shifted viewpoint. A developmental amnesic case with focal bilateral hippocampal pathology showed a massive additional impairment when tested from the shifted viewpoint compared with a mild, list length-dependent, impairment when tested from the same viewpoint. While the same-view condition could be solved by visual pattern matching, the shifted-view condition requires a viewpoint independent representation or an equivalent mechanism for translating or rotating viewpoints in memory. The latter mechanism was indicated by control subjects' response latencies in the shifted-view condition, although the amnesic case is not impaired in tests of mental rotation of single objects. These results show that the human hippocampus supports viewpoint independence in spatial memory, and suggest that it does so by providing a mechanism for viewpoint manipulation in memory. In addition, they suggest an extremely sensitive test for human hippocampal damage, and hint at the nature of the hippocampal role in episodic recollection.

Adult↗
PubMed1997

The role of attention in a spatial memory task in Alzheimer disease patients.

Memory and attention are interrelated cognitive processes that most likely influence the functioning of each other, yet they are often difficult to distinguish in psychological experiments. Young, aged adults, and patients with Alzheimer disease (AD) were tested on a delay response task measuring spatial memory that also placed high demands on attentional resources. Aged adults performed as well as young, suggesting that neither attentional nor memory abilities were exceeded in either group. However, AD subjects were severely impaired on this task. Two further experiments with AD patients examined the relative contribution of attentional and memory deficits in the performance of this population. Both memory and attentional impairments were found; however, errors due to memory factors were more closely related to severity of disease as measured on the Folstein Mini-Mental State Examination than were errors of attentional origin. These studies demonstrate the necessity of accounting for attentional components in studies examining memory, especially in patients with AD.

Adult↗
PubMed2006

The boundary vector cell model of place cell firing and spatial memory.

We review evidence for the boundary vector cell model of the environmental determinants of the firing of hippocampal place cells. Preliminary experimental results are presented concerning the effects of addition or removal of environmental boundaries on place cell firing and evidence that boundary vector cells may exist in the subiculum. We review and update computational simulations predicting the location of human search within a virtual environment of variable geometry, assuming that boundary vector cells provide one of the input representations of location used in mammalian spatial memory. Finally, we extend the model to include experience-dependent modification of connection strengths through a BCM-like learning rule - the size and sign of strength change is influenced by historic activity of the postsynaptic cell. Simulations are compared to experimental data on the firing of place cells under geometrical manipulations to their environment. The relationship between neurophysiological results in rats and spatial behaviour in humans is discussed.

Action Potentials↗
PubMed1995

Spatial memory of body linear displacement: what is being stored?

The ability to evaluate traveled distance is common to most animal species. Head trajectory in space is measured on the basis of the converging signals of the visual, vestibular, and somatosensory systems, together with efferent copies of motor commands. Recent evidence from human studies has shown that head trajectory in space can be stored in spatial memory. A fundamental question, however, remains unanswered: How is movement stored? In this study, humans who were asked to reproduce passive linear whole-body displacement distances while blindfolded were also able to reproduce velocity profiles. This finding suggests that a spatiotemporal dynamic pattern of motion is stored and can be retrieved with the use of vestibular and somesthetic cues.

Acceleration↗
PubMed2004

Low-density lipoprotein receptor-knockout mice display impaired spatial memory associated with a decreased synaptic density in the hippocampus.

The low-density lipoprotein receptor (LDLR) is the first described receptor for apolipoprotein E (apoE). We hypothesize that the absence of the LDLR, similar to the absence of apoE, results in impaired learning and memory processes. Six-month-old homozygous Ldlr-/- and wild-type littermates (Ldlr+/+), maintained on a standard lab chow diet, were used. Unlike humans, Ldlr-/- mice, under these conditions, do not develop atherosclerosis. The results of the Morris water escape task revealed an impaired spatial memory in the Ldlr-/- mice in comparison with Ldlr+/+ mice. Also in a T-maze task, the working memory performance of the Ldlr-/- mice was impaired. Furthermore, Ldlr-/- mice, in comparison with Ldlr+/+ mice, display a decreased number of synaptophysin-immunoreactive presynaptic boutons in the hippocampus CA1. In conclusion, the results show in mice deficiency for the LDLR results in impaired hippocampal-dependent memory functions. A decrease in the number of presynaptic boutons may underlay these behavioral alterations. Therefore, the LDLR may be an important receptor for apoE in the central nervous system.

Animals↗
PubMed2005

The CRH1 antagonist CP154,526 failed to alter ischemia-induced neurodegeneration and spatial memory deficits in rats but inhibited behavioral activity in the novel open field.

Corticotropin-releasing hormone (CRH) has been implicated in ischemia-induced neurotoxicity, due in part to excitatory effects at the hippocampus, and the demonstrated neuroprotective effects of centrally administered, non-specific CRH antagonists. However, a number of issues remain to be clarified from these studies, including the relative contribution of CRH receptor subtypes, and the efficacy of these compounds to alter ischemia-induced behavioral impairments. In the current study, a highly selective, systemically administered CRH1 antagonist (CP154,526) failed to reverse global ischemia-induced cell death in hippocampal CA1 neurons or spatial memory impairments as assessed in the radial arm maze. Similarly, central administration of alpha-helical CRH failed to confer protection against ischemic damage. Interestingly, CRH1 antagonism reversed ischemia-induced hyperactivity in a novel open field, suggesting that modulation of this behavior is independent of effects on hippocampal CA1 cell loss. Failure of the current study to demonstrate neuroprotective effects of either the selective or non-selective CRH antagonists tested challenges the proposed neurotoxic role of CRH in global ischemia. These findings are discussed in relationship to recent findings reconsidering the participation of CRH in excitotoxic-mediated cellular damage.

Animals↗
PubMed1998

Excitotoxic lesions centered on perirhinal cortex produce delay-dependent deficits in a test of spatial memory.

Rats with bilateral electrolytic or ibotenic acid lesions that were centred in perirhinal cortex displayed a significant delay-dependent deficit on a delayed nonmatch to position task in the T maze. Although the removal of prominent extramaze visual cues did not affect the performance of these rats, rotating the maze between the sample and test phases did, indicating that rats were using a spatial strategy. Interestingly, a further group of rats with hippocampal and perirhinal damage displayed deficits that may reflect a dysfunction in the use of inertial cues. These results suggest that both electrolytic and excitotoxic lesions of perirhinal cortex produce spatial memory impairments but that these impairments are qualitatively different than those exhibited following hippocampal damage.

Analysis of Variance↗
PubMed2004

Spatial memory and perspective taking.

Giving directions or describing an environment often requires assuming perspectives other than one's own. We employed a spatial perspective-taking task to investigate how describing familiar versus novel perspectives affects subsequent memory. One participant (the director) viewed a display of objects from a single perspective and described the display to another participant (the matcher) from a perspective that varied by 0 degrees, 45 degrees, 90 degrees, 135 degrees, or 180 degrees from the viewing perspective. Following the description, we assessed the director's memory for the display, using judgments of relative direction, scene recognition, and map drawing. The participants imagined and recognized familiar views faster and/or more accurately than novel views. Moreover, different tasks showed different degrees of facilitation for the visually perceived and described views, suggesting multiple representations for different aspects of spatial memory. These findings emphasize the importance of understanding distinctions among spatial experiences and underscore differences in the tasks used to probe spatial memory.

Female↗
PubMed2005

Spatial memory in middle-aged female rats: assessment of estrogen replacement after ovariectomy.

Previous studies have shown that estrogen influences diverse aspects of neuronal function and morphology and modulates acquisition of various memory tasks in young adult female rodents. It is not clear whether estrogen is critical for optimal memory function in middle-aged female animals, i.e. when cyclicity gradually declines. We trained young adult (5 months) and older (10 months) female Long-Evans rats on a win-shift (delay) 12-arm radial maze (7 arms blocked pre-delay). Rats were preoperatively trained to criterion (< or =2 errors/trial for 3 days) with no delay then with a 60 s delay. All rats were ovariectomized when the age groups were 9 (Y) and 14 months (MA), respectively. Following recovery and retraining to criterion, each rat underwent consecutive treatment cycles with vehicle (Oil) or 17-beta-estradiol benzoate (E). Each 6-day acute treatment cycle, modeled after protocols previously shown to induce morphological and electrophysiological plasticity in the hippocampus at 24-48 h after estrogen injection, consisted of two consecutive daily injections of 10 microg E or Oil (0.1 ml subcutaneously) on Days 1-2 (Oil-Oil or E-E), testing on Days 3-4 at 60 s or 6 h delays, with Days 5-6 comprising of washout days. Each rat received a total of 4 treatment cycles, alternating between Oil and E cycles, in counterbalanced order. Estrogen treatment had no effect in either age group on pre-delay or post-delay errors at either 60 s or 6 h delays. The data indicate that the cyclic estrogen replacement regimen does not influence spatial memory function in young or middle-aged animals in the hippocampal-dependent appetitive radial maze task. Discussion of these unexpected results includes consideration of important experimental design factors that differ between our study and some previous reports, such as the extensive training and task experience our subject received prior to testing for estrogen effects.

Age Factors↗
PubMed2004

Electrolytic lesions of the ventral subiculum weakly alter spatial memory but potentiate amphetamine-induced locomotion.

Adult Long-Evans male rats were subjected to electrolytic lesions of the ventral subiculum, and tested for locomotor activity in the home cage, reference and working memory in the water maze, working memory in the radial maze, and D-amphetamine-induced locomotion (1mg/kg, i.p.). When compared to their sham-operated counterparts, lesioned rats showed nocturnal hyperactivity, no reference memory deficit, but working memory was impaired in the water maze and during the initial stage of radial-maze testing. Their locomotor responsiveness to D-amphetamine was exaggerated. Histological verifications confirmed lesions in the ventral subiculum. Material stained for acetylcholinesterase activity indicated septohippocampal and commissural/associational sprouting, accounting for partial damage to the perforant paths. These results showed that ventral subiculum lesions (i) do not alter the capability of rats to learn repeatedly presented spatial information, and (ii) impair, but do not prevent, spatial working memory, suggesting that the ventral subiculum is preferentially involved in short-term memory for spatial locations. Given the electrolytic nature of the lesion, the lesion-induced potentiation of the locomotor response to amphetamine is probably easier explained by partial disruption of the perforant paths than by damage to neurons of the ventral subiculum.

Acetylcholinesterase↗
PubMed1994

Spatial memory in the desert kangaroo rat (Dipodomys deserti).

Desert kangaroo rats (Dipodomys deserti) forage for seed distributed in patches in the desert environment and may remember patch locations. In Experiment 1, 7 desert kangaroo rats that had discovered the location of a plastic token in 1 box accurately dug for a token hidden in the same location in a 2nd identical box. Results of Experiment 2 indicated that the rats primarily remembered the spatial location of the token within the box in relation to extramaze objects and the walls of the experimental box. Female rats also remembered the chip's location in relation to objects inside the box, but males did not. Experiment 3 demonstrated that the rats' ability to locate the buried token did not depend on detection of the odor of the token. In the discussion I propose that spatial memory in kangaroo rats may have evolved as a result of an overall change in the ontogeny of the species rather than as a specialized adaptation for foraging efficiency.

Animals↗
PubMed2005

Characterizing functional hippocampal pathways in a brain-based device as it solves a spatial memory task.

Analyzing neural dynamics underlying complex behavior is a major challenge in systems neurobiology. To meet this challenge through computational neuroscience, we have constructed a brain-based device (Darwin X) that interacts with a real environment, and whose behavior is guided by a simulated nervous system incorporating detailed aspects of the anatomy and physiology of the hippocampus and its surrounding regions. Darwin X integrates cues from its environment to solve a spatial memory task. Place-specific units, similar to place cells in the rodent, emerged by integrating visual and self-movement cues during exploration without prior assumptions in the model about environmental inputs. Because synthetic neural modeling using brain-based devices allows recording from all elements of the simulated nervous system during behavior, we were able to identify different functional hippocampal pathways. We did this by tracing back from reference neuronal units in the CA1 region of the simulated hippocampus to all of the synaptically connected units that were coactive during a particular exploratory behavior. Our analysis identified a number of different functional pathways within the simulated hippocampus that incorporate either the perforant path or the trisynaptic loop. Place fields, which were activated by the trisynaptic circuit, tended to be more selective and informative. However, place units that were activated by the perforant path were prevalent in the model and were crucial for generating appropriate exploratory behavior. Thus, in the model, different functional pathways influence place field activity and, hence, behavior during navigation.

Animals↗
PubMed2001

Effects of vasopressin on histamine H(1) receptor antagonist-induced spatial memory deficits in rats.

The effects of [Arg(8)] vasopressin on histamine H(1) receptor antagonist-induced memory deficits were investigated using the eight-arm radial maze performance test in rats. Pyrilamine and diphenhydramine as well as scopolamine induced memory deficits characterized by increases in the number of total errors, reference memory errors and working memory errors. [Arg(8)] vasopressin improved not only scopolamine--but also pyrilamine--and diphenhydramine-induced memory deficits, although a high dose of [Arg(8)] vasopressin was needed to antagonize pyrilamine-induced memory deficits. The effects of pyrilamine on the brain [Arg(8)] vasopressin content were studied, and the hippocampus [Arg(8)] vasopressin content was shown to be decreased after pyrilamine injection. From these observations, it seems likely that [Arg(8)] vasopressin participates in not only the cholinergic system but also the histaminergic system in spatial memory.

Animals↗
PubMed2005

The hippocampus, spatial memory and food hoarding: a puzzle revisited.

Behavioural ecology assumes that cognitive traits and their underlying neural substrates are shaped by natural selection in much the same way as morphological traits are, resulting in adaptation to the natural environment of the species concerned. Recently, however, the 'neuroecology' approach of attempting to gain insight into brain structure and function by testing predictions about variation in brain structure based on knowledge of the lifestyle of the animal has been criticized on the grounds that such an adaptationist view cannot provide insight into the underlying mechanisms. Furthermore, the criticism has focussed on attempts to use variation in demand for spatial memory and in hippocampal size as a basis for predicting variation in cognitive abilities. Here, we revisit this critique against the field of so-called 'neuroecology' and argue that using knowledge of the natural history of animals has lead to a better understanding of the interspecific variation in spatial abilities and hippocampal size, and to the generation of novel hypotheses and predictions.

Journal Article↗
PubMed1992

Spontaneous recovery of deficits in spatial memory and cholinergic potentiation of NMDA in CA1 neurons during chronic lithium treatment.

The therapeutic action of lithium in affective disorders is still unclear. One effect of lithium is to deplete membrane inositol and consequently to exhaust the phosphoinositide (PI) pathway. Under chronic lithium treatment, rats showed persistent performance deficits in an active avoidance task and in a visually cued maze. The same treatment, however, resulted in only a transient deficit in the performance of rats in a spatial memory task. Lithium treatment caused a similarly transient deficit in the ability of acetylcholine to potentiate responses to N-methyl-D-aspartate (NMDA) in neurons of the hippocampal slice. The authors propose that the development of compensatory mechanisms may account for the lack of severe memory impairments during lithium treatment. It is suggested that the effects of lithium on the PI pathway are not sufficient to explain the behavioral consequences of chronic lithium treatment.

Acetylcholine↗
PubMed2000

Ca2+-independent phospholipase A2 inhibitor impairs spatial memory of mice.

Pharmacological blockade of Ca2+-independent phospholipase A2 (PLA2) is reported to disintegrate hippocampal synaptic plasticity, which is thought to be the cellular mechanism underlying learning and memory. Therefore, we investigated the effect of the Ca2+-independent PLA2 inhibitor bromoenol lactone (BEL) on spontaneous alteration behaviors of mice. When 3 nmol BEL was intracerebroventricularly injected 30 min prior to the test, the mice showed a poor alternation ratio, compared with control animals. The data suggest that Ca2+-independent PLA2 activity is required for spatial memory.

Animals↗
PubMed2003

Spatial memory impairment in OLETF rats without cholecystokinin - a receptor.

Cholecystokinin (CCK) is one of the most abundant neurotransmitter peptides in the brain. As Otsuka Long-Evans Tokushima Fatty (OLETF) rats lack CCK-A receptor because of a genetic abnormality, we examined whether learning and memory were impaired in these animals using both Morris water maze (MWM) and step-through type passive avoidance (PA) learning test. In the MWM test, memory impairment was observed in OLETF rats. The number of errors was also significantly higher, and that of the correct choices was significantly lower in OLETF rats compared to the controls [Long-Evans Tokushima Otsuka (LETO)] rats. In PA, OLETF rats did not show facilitating response 24 h after training. From these observations, we concluded that a spatial memory was impaired in the OLETF rats.

Animals↗
PubMed1988

Pre- and postnatal choline supplementation produces long-term facilitation of spatial memory.

Although research has demonstrated that short-term improvement in memory function of adult rats can occur when the availability of precursors for the neurotransmitter acetylcholine is increased, little is known about whether memory function of adult rats can be permanently altered by precursor supplementation during early development. In the present study, male albino rats were exposed to choline chloride supplementation both prenatally (through the diet of pregnant rats) and postnatally (subcutaneous injections). At 60 days of age rats were tested on a 12- and 18-arm radial maze task. Results indicated that compared to control littermates, perinatal choline-treated rats showed more accurate performance on both working and reference memory components of the task. This performance difference was apparent on the first block of sessions and continued throughout training. Further analysis revealed that the difference between choline and control rats is not due to use of differential response or cue-use strategies. Instead, it appears that choline induced performance differences are due to long-term enhancement of spatial memory capacity and precision.

Animals↗