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PubMedDate not supplied

Effects of chronic, low-level organophosphate exposure on delayed recall, discrimination, and spatial learning in monkeys and rats.

Chronic exposure to low levels of organophosphate (OP) compounds impairs acetylcholine (ACh) degradation by acetylcholinesterase (AChE) and, in humans, may produce lasting neurotoxicity affecting cognitive function. The present studies examined the ability of such exposure to impair performance of well-learned cognitive tasks in two species, nonhuman primates and rats. During 25 days of exposure to a 0.01 mg/kg dose of the OP diisopropylfluorophosphate (DFP), mature adult monkeys were not impaired in their performance of a well-learned delayed matching-to-sample task (DMTS). However, erythrocyte AChE activity was reduced from predrug levels by 76.26 +/- 3.33% by 14 days after the initiation of DFP administration. Following titration of DFP to a 0.015 mg/kg dose for 15 days, DMTS performance remained at or above baseline levels. DMTS accuracy was moderately, but not significantly, reduced after titration to a dose of 0.02 mg/kg. However, decrements were associated with mild, overt symptoms of OP toxicity and performance returned to baseline levels after withdrawal from OP exposure. In rats, chronic exposure to a low-dose regimen of DFP (0.25 mg/kg/day for 14 days) impaired the ability to initially learn a spatial navigation task, but did not impair performance of previously learned stimulus discrimination and spatial navigation tasks. These data indicate that performance of memory tasks dependent upon reference concepts is not impaired by OP exposure regimens that impair acquisition of novel cognitive tasks prior to the onset of overt toxicity.

Animals↗

PubMed1999

Pretraining prevents spatial learning impairment after saturation of hippocampal long-term potentiation.

Spatial learning is impaired by NMDA receptor antagonists at doses that block hippocampal long-term potentiation (LTP). The deficit is not observed in animals that have received spatial or nonspatial pretraining in a different water maze. To determine whether this conditional impairment reflects debilitating sensorimotor effects of NMDA receptor antagonists in na¿ve animals, we compared spatial learning in na¿ve and pretrained animals in which induction of LTP was blocked by a saturation procedure with no obvious effects on sensorimotor functions. Rats with unilateral hippocampal lesions were implanted with multiple bipolar stimulation electrodes in the angular bundle and a recording electrode in the dentate gyrus of the intact hemisphere. Half of the rats were pretrained to find a hidden platform in a water maze. A week later, pretrained and na¿ve rats received either high-frequency (HF) or low-frequency (LF) stimulation at 2 hr intervals, until no further LTP could be induced. The stimulation did not interefere with performance on a balance task or a visual platform task. After stimulation, all rats were trained in a second water maze. Whereas na¿ve HF animals were impaired, pretrained HF animals acquired the new task rapidly and searched as extensively around the platform as LF control animals. These results suggest that pretraining prevents disruption of spatial learning after saturation of LTP in the absence of sensorimotor impairment, that hippocampal LTP might not be crucial for spatial representation per se, and that LTP may be involved only when spatial and contextual or procedural learning take place simultaneously.

Animals↗

PubMed1992

Chronic neonatal MK-801 treatment results in an impairment of spatial learning in the adult rat.

Chronic neonatal treatment with the non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 from postnatal day 8 through 19 has been shown to affect hippocampal NMDA receptor function of adult rats. Since many studies have shown that NMDA receptors play a crucial role in learning and memory, and since one of the hippocampal functions is spatial learning, we have examined whether this changed response of hippocampal neurons is associated with changes in its normal function. We therefore tested spatial learning and memory using a water maze in adult rats neonatally treated with MK-801. MK-801-treated rats were able to learn the spatial task as well as control rats but at a significantly slower rate. Performance in a visual cue task was not affected by the neonatal treatment, suggesting that the slower spatial learning is not caused by locomotor or sensory deficits. These results suggest that chronic NMDA receptor blockade during the neonatal period leads to long-lasting disturbances of hippocampal function.

Animals↗

PubMed1999

Spatial learning of an escape task by young corn snakes, Elaphe guttata guttata.

Spatial learning is critical to most animals for many behaviours necessary to survival. In vertebrates, most studies on spatial learning and memory have been conducted in mammalian and avian species with few studies on reptiles. We examined spatial learning in the corn snake, Elaphe guttata guttata by training 17 young snakes to find the one open shelter in an eight-hole arena, where the entrance was not visible from the arena surface. Over a 16-trial, 4-day training period, snakes showed (1) a significant decrease in the mean latency to the goal, (2) a significant decrease in the mean total distance travelled, (3) a significant increase in the percentage of the total distance travelled in the quadrant containing the goal, and (4) a significant increase in movement in the goal quadrant above chance. Although no differences were found in the number of errors made over the training period, snakes made fewer errors on all days than expected by chance. This study shows that snakes can learn rapidly a spatial-escape task that is relevant behaviourally and suggests that entering a shelter reinforces this learning. Mechanisms of orientation for the task described are discussed. Copyright 1999 The Association for the Study of Animal Behaviour.

Journal Article↗

PubMed1993

Spatial learning impairment parallels the magnitude of dorsal hippocampal lesions, but is hardly present following ventral lesions.

The hippocampus plays an essential role in spatial learning. To investigate whether the whole structure is equally important, we compared the effects of variously sized and localized hippocampal aspiration lesions on spatial learning in a Morris water maze. The volume of all hippocampal lesions was determined. Dorsal hippocampal lesions consistently impaired spatial learning more than equally large ventral lesions. The dorsal lesions had to be larger than 20% of the total hippocampal volume to prolong final escape latencies. The acquisition rate and precision on a probe test without platform were sensitive to even smaller dorsal lesions. The degree of impairment correlated with the lesion volume. In contrast, the lesions of the ventral half of the hippocampus spared both the rate and the precision of learning unless nearly all of the ventral half was removed. There was no significant effect of the location (dorsal or ventral) of damage to the overlying neocortex only. In conclusion, the dorsal half of the hippocampus appears more important for spatial learning than the ventral half. The spatial learning ability seems related to the amount of damaged dorsal hippocampal tissue, with a threshold at about 20% of the total hippocampal volume, under which normal learning can occur.

Animals↗

PubMed1992

Bilateral knife cuts to the perforant path disrupt spatial learning in the Morris water maze.

Both the hippocampus and the entorhinal cortex are known to be crucial for spatial learning, but the contribution of the pathway linking the two structures, the perforant path (PP), has never been tested in a spatial learning paradigm. The present study examined the role of the PP in spatial learning using the Morris water maze. Seven days after bilateral transection of the PP with a fine-bladed knife, rats were habituated to the pool, then trained to swim from varying start locations to a platform submerged in a fixed location. After 28 training trials over 5 days, probe trials (without any platform present) were given to assess spatial memory for the location. Compared to sham-operated controls, lesioned rats showed slower learning and poorer asymptotic performance in terms of both swim path distance and escape latency, and less preference for the correct quadrant during probe trials. When the platform location was "reversed" to the opposite quadrant, the lesioned rats again showed poorer learning, poorer asymptotic performance, and reduced preference for the correct quadrant on the probe trial. When tested with a visible platform whose position varied from trial to trial, lesioned rats performed as well as controls. These results are congruent with previous analyses of the contributions of the entorhinal cortex and hippocampus to spatial learning and suggest that for spatial learning, the PP is a critical functional link between these two structures.

Animals↗

PubMed1995

Inter-session delay and its effects on performance and retention of spatial learning on a radial maze with mice.

Spatial learning on the radial maze was studied in two inbred strains of mice (C57BL/6 and DBA/2). Five different periods of delay (no delay, 40 min, 2, 8, and 24 h) were inserted between sessions in order to analyze the role of this inter-session delay on training and on retest 1 month later. Results showed that learning profiles and performance levels varied widely with inter-session delay. When the delay was very short (no delay and 40 min), mice of both strains were incapable of learning the task but when the delay was more than or equal to 2 h, the mice succeeded very quickly. The inter-session delay also influenced the performance of mice in the 1-month retention test. C57BL/6 mice obtained good performances in the procedure including a 2-h inter-session delay, while DBA/2 mice obtained good performances with 2- and 8-h delays. These results demonstrate the importance of the procedure in complex spatial learning.

Animals↗

PubMed2002

Spatial learning and synaptic hippocampal plasticity in type 2 somatostatin receptor knock-out mice.

Somatostatin is implicated in a number of physiological functions in the CNS. These effects are elicited through the activation of at least five receptor subtypes. Among them, sst2 receptors appear the most widely expressed in the cortex and hippocampal region. However, the specific role of this somatostatin receptor subtype in these regions is largely undetermined. In this study, we investigated the role of the sst2 receptor in the hippocampus using mice invalidated for the sst2 gene (sst2 KO mice). Complementary experimental approaches were used. First, mice were tested in behavioral tests to explore the consequences of the gene deletion on learning and memory. Spatial discrimination learning in the radial maze was facilitated in sst2 KO mice, while operant learning of a bar-pressing task was slightly altered. Mice were then processed for electrophysiological study using the ex vivo hippocampal slice preparation. Extracellular recordings in the CA1 area showed an enhancement in glutamatergic (AMPA and NMDA) responses in sst2 KO mice which displayed an increase in the magnitude of the short-term potentiation and long-term depression. In contrast, long-term potentiation was not significantly altered. Taken together, these data demonstrate that somatostatin, acting via sst2 hippocampal receptors, may contribute to a global decrease in glutamate efficiency and consequently alter glutamate-dependent plasticity and spatial learning.

Animals↗

PubMed1994

Effects of acute alcohol administration on verbal and spatial learning.

The effects of alcohol and placebo on cognitive functioning in male, Asian-American college students were evaluated with a double-blind, placebo-controlled cross-over design using a multi-trial learning test in which verbal and spatial learning were simultaneously assessed. Verbal recall was impaired consistently across learning trials, while impairment of spatial recall was evident only on later learning trials. Recall of spatial information was influenced by order of presentation and amount of exposure time of items. Results do not support a theory that spatial learning is more impaired by alcohol than verbal learning, and thus do not lend support for the hypothesis that alcohol has a greater effect on right than left hemisphere functioning. Results provide evidence that alcohol increases susceptibility to interference effects.

Adult↗

PubMed2002

Hippocampal expression of c-fos is not essential for spatial learning.

The formation of long-term memory is thought to involve underlying changes in synaptic strength. Many studies have focused on the mechanisms of spatial learning behavior in mammals that is critically dependent on the proper function of the hippocampus. Because of the enduring nature of long-term memory, it is thought that gene expression is involved in this process. The immediate early gene (IEG) c-fos encodes a transcription factor. The c-Fos proteins form heterodimeric proteins with the c-Jun family proteins and the resulting AP-1 transcription complex plays a key role in coupling short-term events elicited by stimuli received at the cell membrane to long-term neuroplastic changes by regulating gene expression. c-fos is induced in the hippocampus after spatial learning. Despite this knowledge, the precise role of c-fos in memory formation and the underlying mechanisms remain unknown. To start investigating the role of c-fos in learning and memory and underlying mechanisms, we evaluated spatial learning capabilities using mice carrying a hippocampal region-specific mutation of c-fos. We found that the c-fos mutant mice exhibit normal spatial learning behaviors in both the Morris water maze and the Barnes maze tests compared to control mice. Our results suggest that hippocampal c-fos expression is not essential for spatial learning.

Animals↗

PubMed1999

The effects of lesions to the caudolateral neostriatum on sun compass based spatial learning in homing pigeons.

To better define the role of the avian caudolateral neostriatum (NCL) in spatial behavior, we used homing pigeons to explore the effects of NCL lesions on a sun compass based spatial learning task. Although NCL lesioned birds learned the task, they required more sessions to reach criterion than controls. NCL lesioned pigeons were also able to acquire a color discrimination task that was procedurally similar to the sun compass spatial learning task, but they made more errors than controls. Both the deficits observed in sun compass based spatial learning and color discrimination were correlated with the volume of lesion damage to dorsal rather than ventral portions of NCL. Overall, these findings suggest that the role of NCL in homing pigeon navigation from distant unfamiliar locations is not related to a bird's ability to learn stimulus-direction associations using a sun compass. However NCL does appear involved in a pigeon's ability to perform at least some behaviors common to both the color discrimination and the sun compass based spatial learning tasks.

Animals↗

PubMed1993

Visual-spatial learning in nonalcoholic young adults with and those without a family history of alcoholism.

Visual-spatial learning in young adult nonalcoholic men and women with (FH+) and those without (FH-) a family history of alcoholism was investigated using nonsense shapes of high and low verbal association value. Four groups of FH+ and FH- men and women, 16 subjects in each group, were tested. The male FH+ group required significantly more trials to reach learning criterion and made more errors than the male FH- group; the FH effect was not significant in females although similar trends were present. Women exhibited significantly poorer visual-spatial learning compared to the men. High compared to low verbal association shapes were learned in fewer trials with fewer errors by all groups. There were no significant FH by verbal association interactions, indicating that the impaired visual-spatial learning in the FH+ men could not be ascribed to the meaningfulness dimension of the nonsense shapes. These results suggest that the impaired visual-spatial learning found in adult children of alcoholics (ACOAs) might be due in part to premorbid cognitive deficits.

Adolescent↗

PubMed1993

Effects of intracranial infusions of chlordiazepoxide on spatial learning in the Morris water maze. II. Neuropharmacological specificity.

In the preceding paper it was found that infusions of chlordiazepoxide (CDP) into the medial septal region, but not several other regions possessing a high density of benzodiazepine receptors, impaired spatial learning, but not cue learning or swim speed, in the Morris water maze. The present investigation sought to further characterize the neuropharmacological profile of this effect. Initially, it was reconfirmed that systemically administered CDP impaired spatial learning, but not cue learning or swim speed, in the water maze. Additionally, it was found that systemically administered scopolamine, a muscarinic antagonist, impaired both spatial and cue learning, but not swim speed, confirming the detrimental effects of cholinergic hypofunction on maze learning. In new rats, a dose-response assessment revealed that 60 and 30 nmol, but not 10 nmol, CDP infused into the medial septum impaired spatial learning, but not cue learning or swim speed. On the following day, rats from each dose group, now undrugged, acquired a reversed platform location at control levels, suggesting that the previously observed impairment was not due to a neurotoxic effect. Additionally, it was found that systemically administered flumazenil (10 mg/kg) blocked the spatial learning deficit produced by the 60 nmol dose of CDP infused into the medial septum. However, intraseptal infusions of flumazenil (10, 20, or 30 nmol) failed to attenuate the spatial learning deficit produced by systemically administered CDP. Finally, systemically administered tetrahydroaminoacridine (1 or 3 mg/kg), an acetylcholinesterase inhibitor, failed to attenuate the spatial learning deficit produced by intraseptal CDP (60 nmol). Together these results implicate benzodiazepine receptors in the medial septum in the amnesic actions of CDP but suggest that additional sites also mediate this action. The present results fail to support the idea that the spatial learning deficit produced by intraseptal infusions of CDP is due to a suppression of septo-hippocampal cholinergic activity and it is proposed that CDP impairs spatial learning by exacerbating hippocampal inhibition by inhibiting septo-hippocampal GABAergic projection neurons.

Animals↗

PubMed1994

Genetic and activity-dependent regulation of zif268 expression: association with spatial learning.

We have reported that C57BL/6 and DBA/2 mice differ in spatial learning performance and associated hippocampal protein kinase C (PKC) activity (Upchurch and Wehner, 1989, Behav Neurosci 103:1251-1258; Wehner et al., 1990, Brain Res 523:181-187) and that physical activity enhances spatial learning with related alterations in protein kinase C (PKC) (Fordyce and Wehner, 1993b, Brain Res 619:111-119). To assess whether physical activity induces alterations in gene expression that may underlie these changes in PKC and learning performance, we examined the effect of physical activity on expression of zif268, a transcription regulatory factor linked to stimulus-induced neuronal plasticity. C57 and DBA mice, 3 months of age, were subjected to acute (one bout) or chronic (8 weeks) physical activity. The mice were then tested on the Morris water maze task for 6 days with subsequent analysis of PKC activity and zif268 mRNA expression. Control DBA mice, which have poor hippocampal-specific learning performance compared to C57 mice (Wehner et al., 1990, Brain Res 523-181-187; Fordyce and Wehner, 1993b, Brain Res 619:111-119; Paylor et al., 1993, Psychobiology 27:11-26), displayed lower basal levels of zif268 mRNA (P < .05). As observed previously, chronic physical activity produced an enhancement in spatial learning performance accompanied by alterations in hippocampal PKC activity in both strains of mice (P < .05). In addition, the present investigation demonstrated that acute physical activity increased mRNA levels of zif268 in hippocampal regions CA1, CA3 and overlying cortex (P < .005) of both C57 and DBA mice. Chronic physical activity suppressed the basal expression of zif268 in C57 mice in CA1 and overlying cortex below control levels. These findings suggest that genetic and activity-dependent regulation of zif268 may influence learning performance.

Animals↗

PubMed2006

[Effect of citicoline on spatial learning and memory of rats after focal cerebral ischemia].

OBJECTIVE: To investigate the effects of citicoline on spatial learning and memory of rats after focal cerebral ischemia. METHODS: The rats were randomly divided into sham-operation group, ischemia control group and citicoline group. In the later two groups, focal cerebral ischemia model was established by introducing an intraluminal filament into the left middle cerebral artery, and citicoline (500 mg/kg) or 0.9% NaCl was administered intraperitoneally once a day for 2 weeks after the operation. The rats in the sham-operation group were not subjected to middle cerebral artery occlusion (MCAO) with intraluminal filament. The spatial learning and memory functions of the rats were evaluated by Morris water maze test 15 days after MCAO for 5 days. RESULTS: The rats in ischemia control group exhibited serious spatial learning and memory deficits in both place navigation test and spatial probe test. In the former test, the mean escape latency of citicoline-treated rats were significantly shorter than that of ischemia control rats (P<0.01), and in the latter test significant diffidence was noted between citicoline and ischemia control groups in the percentage time spent in the former platform quadrant and frequency of crossing the former platform (P<0.05). CONCLUSION: Citicoline can improve the spatial learning and memory function of rats after focal cerebral ischemia.

Animals↗

PubMed2006

Spatial learning deficits induced by chronic prenatal ethanol exposure can be overcome by non-spatial pre-training.

UNLABELLED: This study tested the hypothesis that behavioural intervention, in the form of non-spatial pre-training, mitigates the deficits in spatial learning tasks induced in guinea pig offspring by chronic prenatal ethanol exposure (CPEE). Timed, pregnant guinea pigs were treated with ethanol (4 g/kg maternal body weight/day), isocaloric-sucrose/pair-feeding, or water throughout gestation. Offspring received non-spatial pre-training, in which animals were exposed to the procedural requirements of the water maze in the absence of distal spatial cues, and then were tested in both stationary-platform and moving-platform tasks with spatial cues. Saliva cortisol was quantified in non-trained and pre-trained animals before and after exposure to the water maze. RESULTS: CPEE offspring exhibited performance deficits in the stationary-platform task, and non-spatial pre-training improved performance of CPEE offspring to control levels. In contrast, non-spatial pre-training had no effect on the impaired performance of CPEE offspring in the moving-platform task. Non-trained CPEE offspring had elevated saliva cortisol concentration after water-maze exposure compared to control offspring. Moreover, pre-trained control animals exhibited a sensitization of the cortisol response after repeated exposure to the water maze, and this was not evident in pre-trained CPEE offspring. CONCLUSIONS: These data demonstrate that CPEE produced deficits in spatial learning and memory processes that were partially overcome by non-spatial pre-training; however, more difficult tasks continued to reveal cognitive deficits. For repeated exposure to the water maze, CPEE offspring achieved a level of performance that was not different from control offspring, suggesting that it is the initial rate of acquisition of new learning, rather than the overall ability to learn, that is most adversely affected by CPEE.

Animals↗

PubMed1996

Baclofen, a selective GABAB receptor agonist, dose-dependently impairs spatial learning in rats.

The present investigation assessed the effects of the selective GABAB receptor agonist baclofen (1, 3, and 6 mg/kg) on spatial learning in the Morris water maze, an aversively motivated spatial learning task. Potential anxiolytic and sedative effects of baclofen were also assessed in an open field. Baclofen dose-dependently reduced locomotion in the open field but had little effect on thigmotaxia (anxiety). In the water maze, baclofen dose-dependently impaired spatial learning and reduced swim speed. During the probe trial given after training, only rats treated with the highest dose of baclofen (6 mg/kg) failed to show a bias for the correct quadrant. Following four additional retraining trials, a second drug-reversal probe trial was given and it was found that rats switched from saline to the highest dose of baclofen (6 mg/kg) showed a bias for the correct quadrant, as did rats switched from the two lowest doses of baclofen (1 and 3 mg/kg) to saline. Rats switched from the highest dose of baclofen (6 mg/kg) to saline failed to show a quadrant bias. Performance on a visible platform task was not impaired by baclofen at any dose. Together these results suggest that baclofen resembles GABAA agonists/positive modulators in that it impairs spatial learning, but not performance of a previously acquired escape response; but differs in that it does not reduce thigmotaxia (anxiety). Potential mechanisms by which baclofen impairs mnemonic processes are discussed.

Animals↗

PubMed2000

Impaired spatial learning in aged rats is associated with loss of p75-positive neurons in the basal forebrain.

We investigated age-related changes in the number and size of neurons positive for the p75 neurotrophin receptor in the cholinergic basal forebrain of female Dark Agouti rats. Since the integrity of these neurons is known to be closely associated with performance in tests of spatial learning ability, we also investigated the incidence of age-related spatial learning impairments, using the Barnes maze. Spatial learning impairments occurred with increasing frequency with age. No rats showed impairment at six months, but 50% were impaired at 14 months and 71% at 26 months. There was no correlation between age and decreased number of p75-positive neurons in the rostral basal forebrain, which consists of the medial septum and vertical limb of the diagonal band of Broca. In the caudal basal forebrain, which consists of the horizontal limb and the nucleus of Meynert, there was a 13% reduction in the number of p75-positive neurons at 17 months compared to six months, and a 30% reduction at 26 months. There was a strong correlation between the presence of spatial learning impairment and a reduction in the number of p75-positive neurons. This correlation was most evident in the rostral basal forebrain, but was also present in the caudal basal forebrain. In the rostral basal forebrain, all learning impaired rats had fewer p75-positive neurons than the average number in unimpaired rats. A close correspondence between the presence of p75 and choline acetyltransferase was evident in basal forebrain neurons of learning-impaired and unimpaired rats. Gross pathological changes to the morphology of p75-positive neurons were relatively frequent in learning-impaired rats. These changes consisted of hypertrophy, appearance of vacuoles, and marginalisation of the cytoplasm. The results indicate the susceptibility of p75-positive neurons to degenerative changes with aging, and show that the loss of these neurons in the basal forebrain was strongly correlated with impairment in spatial learning.

Age Factors↗