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PubMed2006

Prenatal stress modifies hippocampal synaptic plasticity and spatial learning in young rat offspring.

Clinical studies demonstrate that prenatal stress causes cognitive deficits and increases vulnerability to affective disorders in children and adolescents. The underlying mechanisms are not yet fully understood. Here, we reported that prenatal stress (10 unpredictable, 1 s, 0.8 mA foot shocks per day during gestational days 13-19) impaired long-term potentiation (LTP) but facilitated long-term depression (LTD) in hippocampal CA1 region in slices of the prenatal stressed offspring (5 weeks old). Cross-fostering neonate offspring by the prenatal stressed or control mothers did not change the effects of prenatal stress on the hippocampal LTP and LTD. Furthermore, prenatal stress enhanced the effects of acute stress on the hippocampal LTP and LTD and impaired spatial learning and memory in the Morris water maze in the young rat offspring. Therefore, prenatal stress alters synaptic plasticity and enhances the effects of acute stress on synaptic plasticity in the hippocampus, which may be the mechanism for the impaired spatial learning and memory in young rat offspring.

Animals↗
PubMed2007

Impaired spatial learning in the APPSwe + PSEN1DeltaE9 bigenic mouse model of Alzheimer's disease.

Mice co-expressing the Swedish amyloid precursor protein mutation (APP(Swe)) and exon 9 deletion (DeltaE9) of the PSEN1 gene begin to develop amyloid plaques at 6-7 months of age. We demonstrate here a spatial learning deficit in 7-month-old APP(Swe) + PSEN1DeltaE9 bigenic mice using an adaptation of the Barnes maze. Mice were first trained on a cued target followed by a hidden-target condition. Although bigenic mice quickly learned the cued-target version of the task, they were significantly impaired when switched to the hidden-target version. In contrast, a separate group of double-transgenic mice trained first on the spatial hidden-target version of the task were unimpaired relative to wild-type controls. We propose that processes such as general rule learning, context learning and exploratory habituation exert a greater influence when the testing environment is novel and overshadow the spatial memory deficit in naive bigenic mice. However, when cued-target training is conducted first, these processes habituate and the spatial learning deficit is unmasked. Seven-month-old APP(Swe) + PSEN1DeltaE9 mice were unimpaired on tests of memory that did not involve learning the rules governing spatial associations.

Alzheimer Disease↗
PubMed2005

Early amygdala damage disrupts performance on medial prefrontal cortex-related tasks but spares spatial learning and memory in the rat.

Recent studies have demonstrated that the postnatal development of connections between the basolateral amygdala (BLA) and the medial prefrontal cortex (mPFC) mature around postnatal days 13-15 (pd13-15), whereas these between the BLA and other structures such as the nucleus accumbens and the mediodorsal thalamus are completed by pd7. Accordingly, it is hypothesized that mPFC cytoarchitecture and hence its function may be specifically affected by neonatal (i.e. on pd7) but not later induced (i.e. on pd21) damage to the BLA. To test this hypothesis, rats received excitotoxic lesions to the BLA on either pd7 or pd21 and were subjected to two tests putatively sensitive to mPFC dysfunction, namely food hoarding and spontaneous alternation. In addition, rats were tested for spatial learning and memory, to determine any possible effects on hippocampal function. Consistent with the documented effects of mPFC lesions, pd7 damage to the BLA impaired spontaneous alternation and food hoarding performance, an effect that was not found in rats with BLA lesions induced on pd21. Spatial learning and memory, however, were not affected by the (neonatal) lesion procedure. Together, these results indicate that neonatal BLA damage affects species-specific sequential behavior and flexibility, which may be attributed to abnormal functioning of the mPFC.

Amygdala↗
PubMed1998

Altered spatial learning and memory in mice lacking the mGluR4 subtype of metabotropic glutamate receptor.

The glutamate analog, L-2-amino-4-phosphonobutyric acid (L-AP4) is a selective agonist for several members of the metabotropic glutamate receptor (mGluR) family. Activation of presynaptic mGluRs by L-AP4 causes a suppression of synaptic transmission in the central nervous system. In this study, the role of 1 subtype of mGluR in the nervous system was investigated by analyzing mutant mice lacking the L-AP4-sensitive receptor, mGluR4. Experiments designed to probe hippocampal function showed no impairments in acquisition of spatial learning in the water maze task. However, in a spatial reversal learning task, the mutant mice exhibited significantly accelerated learning performance. Furthermore, in a probe trial administered 6 weeks posttraining, these mice showed impaired spatial accuracy. The results suggest that the mutant mice differed in their ability to learn and integrate new spatial information into previously formed memory traces and that their use of stored spatial information also was altered. Thus, the presynaptically expressed mGluR4 plays a role in the processing of spatial information.

Analysis of Variance↗
PubMed2003

Long-term potentiation in the hippocampal CA1 area and dentate gyrus plays different roles in spatial learning.

NMDA receptor-dependent long-term potentiation (LTP) at hippocampal synapses has been considered a crucial component of the cellular basis for learning and memory. This form of LTP occurs in excitatory synapses in both the CA1 area and the dentate gyrus in the hippocampus. However, differential roles of LTP in these areas have not yet been identified. To address this issue, we enhanced the degree of LTP by expressing Ca2+-permeable AMPA receptors at either hippocampal CA1 or dentate gyrus synapses using Sindbis viral vectors (SINs) encoding both green fluorescent proteins and unedited GluR2 (GluR2Q) subunits, and examined their effects on rat spatial learning. The viral vectors were locally injected into the 8-week-old-rat brain in vivo bilaterally. The postsynaptic expression of Ca2+-permeable AMPA receptors enhanced the degree of LTP, and induced NMDA receptor-independent LTP in the presence of the NMDA receptor antagonist in SIN-infected regions in both CA1 and dentate gyrus in hippocampal slice preparations. However, the regional expression of Ca2+-permeable AMPA receptors caused opposite behavioural consequences on the Morris water maze task: rats with SIN-infected CA1 pyramidal cells showed shorter escape latency and better probe test performance, whereas those with SIN-infected dentate gyrus granule cells showed impaired performance. Thus, it was demonstrated that CA1 and dentate gyrus synapses play different functional roles in spatial learning despite their similar mechanism for LTP induction.

Animals↗
PubMed2002

Impaired spatial learning in the Morris water maze induced by serotonin reuptake inhibitors in rats.

The effects of selective serotonin reuptake inhibitors citalopram and fluoxetine on spatial learning were assessed in rats. Adult male rats were subjected to 4 days of training in the Morris water maze with the invisible platform. Animals received different doses of citalopram (1-8 mg/kg; i.p.) or fluoxetine (1-16 mg/kg; i.p.) or their vehicles (saline or distilled water respectively) 30 minutes before training each day. The results showed that citalopram at doses of 4 and 8 mg/kg and fluoxetine at doses of 8 and 16 mg/kg significantly increased latencies to find the platform and traveled distances compared to the control group. Therefore, it appears that selective serotonin reuptake inhibitors can cause learning deficits in complex spatial tasks such as Morris water maze.

Animals↗
PubMed1996

MK-801 neurotoxicity in male mice: histologic effects and chronic impairment in spatial learning.

Several histological and behavioral experiments were conducted to investigate the neurotoxic effects of MK-801 in male mice. Moderate subcutaneous (s.c.) doses of MK-801 (0.5 and 1.0 mg/kg) induced the formation of intracytoplasmic vacuoles in pyramidal neurons in layers III and IV of the posterior cingulate/retrosplenial (PC/RS) cortex in 50% and 100% of the mice from the two respective treatment groups. Electron microscopic analysis of the vacuoles indicated that mitochondria and endoplasmic reticulum are the cellular organelles most prominently involved in this pathomorphological change. Treating mice with a high systemic dose of MK-801 (10 mg/kg s.c. or intraperitoneal (i.p.)) caused selective, irreversible degeneration of a small number of PC/RS cortical neurons. Compared to saline controls, the acquisition performance of mice treated i.p. with 10 mg/kg MK-801 was chronically impaired on a spatial learning task (modified hole board food search task) when tested at several posttreatment intervals (up to at least 5 months), although the groups did not differ on activity or sensorimotor tests conducted 2 weeks posttreatment. In summary, MK-801 caused histopathological changes in the mouse brain similar to those observed in the rat. Furthermore, high dose MK-801 treatment that killed a small number of mouse PC/RS cortical neurons resulted in a chronic acquisition impairment in spatial learning, an effect not previously demonstrated in any species.

Animals↗
PubMed2000

Enlarged cholinergic forebrain neurons and improved spatial learning in p75 knockout mice.

The p75 low affinity neurotrophin receptor (p75) can induce apoptosis in various neuronal and glial cell types. Because p75 is expressed in the cholinergic neurons of the basal forebrain, p75 knockout mice may be expected to show an increased number of neurons in this region. Previous studies, however, have produced conflicting results, suggesting that genetic background and choice of control mice are critical. To try to clarify the conflicting results from previous reports, we undertook a further study of the basal forebrain in p75 knockout mice, paying particular attention to the use of genetically valid controls. The genetic backgrounds of p75 knockout and control mice used in this study were identical at 95% of loci. There was a small decrease in the number of cholinergic basal forebrain neurons in p75 knockout mice at four months of age compared with controls. This difference was no longer apparent at 15 months due to a reduction in numbers in control mice between the ages of 4 and 15 months. Cholinergic cell size in the basal forebrain was markedly increased in p75 knockout mice compared with controls. Spatial learning performance was consistently better in p75 knockout mice than in controls, and did not show any deterioration with age. The results indicate that p75 exerts a negative influence on the size of cholinergic forebrain neurons, but little effect on neuronal numbers. The markedly better spatial learning suggests that the function, as well as the size, of cholinergic neurons is negatively modulated by p75.

Aging↗
PubMedDate not supplied

[Is the hippocampus necessary for spatial learning?].

OBJECTIVE: A variety of findings, mainly based on lesion studies, have led to the proposal that the hippocampus is a necessary component of the neural system supporting spatial learning. However, recent research is challenging this classic view. The goal of this review is to discuss and integrate these new data with previous findings. DEVELOPMENT: Several studies performed in our lab have shown that hippocampal lesions do not affect the acquisition of a place response if a special training procedure is used. Nevertheless, the way how this special training method overcome the learning deficit is not well known. In this review we propose that hippocampal damage produces several non spatial deficit, being one of them a deficit in behavioral flexibility. Thus, it is possible that our special training procedure encourage behavioral flexibility and variability in response in lesioned subjects, which would allow a significant improvement in the learning of the spatial task. CONCLUSION: The data discussed in this review suggest that the hippocampus is not completely necessary for the learning of a place. It would be the sum of spatial and non spatial deficit ('hippocampal syndrome') which would produce the acquisition deficit typically seen in hippocampal rats when a traditional training method is used.

Amnesia↗
PubMed2005

Chronic developmental lead exposure reduces neurogenesis in adult rat hippocampus but does not impair spatial learning.

The dentate granule cell (DG) layer of the hippocampal formation has the distinctive property of ongoing neurogenesis that continues throughout adult life. Although the function of these newly generated neurons and the mechanisms that control their birth are unknown, age, activity, diet and psychosocial stress have all been demonstrated to regulate this type of neurogenesis. Little information on the impact of environmental insults on this process has appeared to date. Developmental lead (Pb) exposure has been well documented to impair cognitive function in children and animals and reduce activity-dependent synaptic plasticity in the hippocampus of rodents. Therefore, we examined the effects of this classic environmental neurotoxicant on hippocampal-dependent learning and adult neurogenesis in the hippocampus. Pregnant rats were exposed to a low level of Pb-acetate (0.2%) via the drinking water from late gestation (GD 16) until weaning on postnatal day 21 (PN 21). At weaning, half of the Pb-exposed animals were weaned to control drinking water and the remainder were maintained on Pb water until termination of the study. Animals were paired- housed and on PN 75 were administered a series of injections of a thymidine analog bromodeoxyuridine (BrdU), a marker of DNA synthesis that labels proliferating cells and their progeny. At 12-h intervals for 12 days, rats received an ip injection of BrdU (50 mg/kg). Subjects were sacrificed and perfused 24 h and 28 days after the last injection. Spatial learning was assessed in an independent group of animals beginning on PN 110 using a Morris water maze. No Pb-induced impairments were evident in water maze learning. Immunohistochemistry for the detection of BrdU-labeled cells was performed on 40-microm coronal sections throughout the hippocampus. Continuous exposure to Pb (Life) reduced the total number of BrdU-positive cells at 28 days without affecting the total number of labeled cells evident 24 h after the last injection. No differences in the number of progenitor cells labeled or surviving were seen between control and treated animals whose Pb exposure was terminated at weaning. Double labeling with BrdU and the glial specific marker, glial acidic fibrillary protein (GFAP) indicated that the bulk of the surviving cells were of a neuronal rather than a glial phenotype. These data reveal that chronic low-level Pb exposure reduces the capacity for neurogenesis in the adult hippocampus. Despite deficits in synaptic plasticity previously reported from our laboratory, and now structural plasticity, no significant impact on spatial learning was detected.

Aging↗
PubMed2002

Long term administration of Hypericum perforatum improves spatial learning and memory in the water maze.

The aim of the present study is to investigate the effects of long-term Hypericum perforatum treatment on spatial learning and memory in rats. Hypericum preparation (HP) standardized to 0.3% hypericin content was administered orally for 9 weeks in doses of 4.3 and 13 microg/kg corresponding to therapeutic dosages in humans of 0.3 and 0.9 mg of total hypericins daily. A Morris water maze paradigm was used. The mean escape latency over 4 d for the Control group (21.9 s) and HP 4.3 group (21.7 s) was significantly greater than the latency of the HP 13 group (15.8s). In the probe trial on day 5, the HP 13 group crossed the correct annulus in the SE quadrant more often (4.5) than the other groups: Con (2.4) and HP 4.3 (3.1). After completion of the behavioral experiment, the regional brain concentrations of monoamines and metabolites were estimated in selected brain regions, i.e. prefrontal cortex, hippocampus and hypothalamus. Analysis of variance (ANOVA) demonstrated significant differences in the content of monoamines and metabolites between the treatment groups compared to the Control. The increased 5-hydroxytryptamine (5-HT) levels in the prefrontal cortex correlated positively with the retention of spatial memory. These findings show that the long-term administration of Hypericum perforatum can improve learning and spatial memory with significant changes in the content of monoamines in several brain regions.

Animals↗
PubMed1995

Sex differences in vulnerability to developmental spatial learning deficits induced by limited binge alcohol exposure in neonatal rats.

The two main objectives of this study were (1) to replicate previous findings that 6 days of binge-like exposure to alcohol during the neonatal brain growth spurt induces significant place learning deficits in juvenile rats and (2) to determine whether more limited (3-day) binge-like exposure during the neonatal period induces place learning deficits and whether the effects depend on the developmental timing of the exposure. Using artificial rearing methods and a split-litter experimental design, groups of male and female neonatal rats were given binge-like exposure to 4.5 g/kg/day of ethanol in milk formula either on Postnatal Days (PD) 4-6, PD 7-9, or PD 4-9, which yielded mean peak blood alcohol concentrations of 230-260 mg/dl. Controls included an artificially reared gastrostomy control group (GC) given an isocaloric milk formula diet on PD 4-9 and a suckle control group reared normally by lactating dams. Acquisition of place learning in the Morris spatial navigation task was trained for 6 consecutive days beginning on PD 26; a probe trial was given at the end of the sixth day. As expected, both males and females given alcohol on PD 4-9 had significant deficits in acquisition and probe trial performance relative to SC and GC groups. Males given the PD 7-9 exposure had significant place learning deficits which were as severe as with the full 6-day exposure. The PD 4-6 exposure in males produced only a nonsignificant trend toward slower acquisition. Females were not significantly affected by either 3-day exposure. The latter phase of the neonatal brain growth spurt appears to constitute a sex-specific period of enhanced vulnerability to alcohol-induced developmental spatial learning deficits.

Animals↗
PubMed1997

Ontogenetic differences in retention of spatial learning tested with the Morris water maze.

Two experiments examined retention of spatial learning in rats using a Morris water maze. Retention was scored in terms of probe trial performance when the platform was removed. Latency to reach the platform location, percent of time in the quadrant that had contained the platform, and relative frequency of visits to the platform location were analyzed. Results of the first experiment showed that preweanlings and juveniles exhibited substantial forgetting at 3- and 7-day retention intervals. Forgetting in adults was much lower than that found in the younger animals, and no differences in amount of forgetting appeared between the 3- and 7-day retention intervals at any age. The second experiment showed that forgetting in juveniles was alleviated by a single training trial administered just prior to the probe trial. These results are discussed in terms of ontogenetic differences in memory processing and measurement issues pertinent to the Morris water maze test procedure.

Aging↗
PubMed1995

Simulation of spatial learning in the Morris water maze by a neural network model of the hippocampal formation and nucleus accumbens.

Cells in the hippocampal formation show spatial firing correlates thought to be critical to the role played by this structure in spatial learning. Place cells in the hippocampus proper show location-specific activity, whereas cells in the postsubiculum fire as a function of momentary directional heading. One question which has received little attention is how these spatial signals are used by motor structures to actually guide spatial behavior. Here we present a model of how one kind of spatial behavior, instrumental learning in the Morris water maze, could be guided by the spatial information in the hippocampal formation. For this, we concentrate on the hippocampal projection to the nucleus accumbens, which is strongly implicated in instrumental learning. In the model, simulated firing patterns of place cells and head direction cells activate "motor" cells in the "accumbens." Each motor cell causes a particular locomotor movement in a simulated rat. In this way, the "rat" locomotes through the simulated environment. Each step places the animal in a slightly different location and directional orientation, which, in turn, activates a different set of place and head direction cells, thus causing the next locomotor response, and so on. Connection strengths between cells are initially set randomly. When the animal encounters the reward location, however, connections are altered, so that recently active synapses are strengthened. Thus, successful moves in a particular locational and directional context are "stamped in." Simulated rats show rapid learning, similar in many ways to that of actual rats. In particular, they generate efficient routes to the goal after minimal experience, and can do so from somewhat novel starting positions. Consideration of the model architecture shows that 1) combined use of directional and place information is an example of a linearly inseparable problem and that 2) some types of novel route generation, often thought to require a "cognitive mapping" strategy, can be generated from the S-R type model used here.

Animals↗
PubMed2003

Spatial and non-spatial learning in turtles: the role of medial cortex.

In mammals and birds, hippocampal processing is crucial for allocentric spatial learning. In these vertebrate groups, lesions to the hippocampal formation produce selective impairments in spatial tasks that require the encoding of relationships among environmental features, but not in tasks that require the approach to a single cue or simple non-spatial discriminations. In reptiles, a great deal of anatomical evidence indicates that the medial cortex (MC) could be homologous to the hippocampus of mammals and birds; however, few studies have examined the functional role of this structure in relation to learning and memory processes. The aim of this work was to study how the MC lesions affect spatial strategies. Results of Experiment 1 showed that the MC lesion impaired the performance in animals pre-operatively trained in a place task, and although these animals were able to learn the same task after surgery, probe test revealed that learning strategies used by MC lesioned turtles were different to that observed in sham animals. Experiment 2 showed that the MC lesion did not impair the retention of the pre-operatively learned task when a single intramaze visual cue identified the goal. These results suggest that the reptilian MC and hippocampus of mammals and birds function in quite similar ways, not only in relation to those spatial functions that are impaired, but also in relation to those learning processes that are not affected.

Animals↗