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PubMed2002

[Learning/memory and drug dependence].

We investigated the possible mechanisms of development of latent learning and morphine dependence by the methods of behavioral pharmacology and confirmed them by using mutant mice. The heterozygous mice for the tyrosine hydroxylase (TH) gene and for the cyclic AMP (cAMP) response element binding protein (CREB) binding protein (CBP) gene showed the impairment of latent learning in the water finding task, and these mice did not develop morphine dependence. The spatial learning and hippocampal long-term potentiation (LTP) were normal in the both mutants. TH heterozygous mice showed a reduction of high K(+)-evoked noradrenaline release in the frontal cortex measured by the microdialysis technique and of cAMP content in the brain. In conclusion, the results of mutant mice suggest that the alternation of catecholamine biosynthesis and cAMP signal pathways may play a key role in development of latent learning and morphine dependence, and they furthermore show that the expression of genes mediated by phosphorylated CREB may be involved in the development of latent learning and morphine dependence.

Animals↗
PubMed2002

Chronic inhibition of glutamine synthetase is not associated with impairment of learning and memory in mice.

The convulsant methionine sulfoximine (MSO) is a byproduct of the agenized flour commonly used for feeding domestic animals decades ago. MSO is a powerful glycogenic and epileptogenic agent, and it is an irreversible inhibitor of glutamine synthetase. This latter effect was hypothesized to be responsible for the increase in the incidence of some neuropathologies in humans, such as Alzheimer's disease or Parkinson's disease. In order to test this hypothesis, we chronically administered MSO to two inbred strains of mice, C57BL/6J and BALB/cJ, and analyzed possible alterations in learning and memory features of these mice. Mice were given 20 mg/kg of MSO three times a week for 10 weeks. Spatial learning capabilities assessed with a radial maze were not affected by the long-term MSO treatment, although activity was significantly decreased in BALB/cJ mice. Thus, our data suggest that long-term administration of non-convulsive and non-glycogenic doses of MSO do not alter the spatial memory of mice. Our results do not support the hypothesis that chronic treatment with MSO influences hippocampus-dependent learning abilities in mice.

Animals↗
PubMed2003

Routes to remembering: the brains behind superior memory.

Why do some people have superior memory capabilities? We addressed this age-old question by examining individuals renowned for outstanding memory feats in forums such as the World Memory Championships. Using neuropsychological measures, as well as structural and functional brain imaging, we found that superior memory was not driven by exceptional intellectual ability or structural brain differences. Rather, we found that superior memorizers used a spatial learning strategy, engaging brain regions such as the hippocampus that are critical for memory and for spatial memory in particular. These results illustrate how functional neuroimaging might prove valuable in delineating the neural substrates of mnemonic techniques, which could broaden the scope for memory improvement in the general population and the memory-impaired.

Adult↗
PubMed2005

Assessment of the effects of the cyclooxygenase-2 inhibitor rofecoxib on visuospatial learning and hippocampal cell death following kainate-induced seizures in the rat.

Kainate-induced seizures result in hippocampal neurodegeneration and spatial learning deficits in rodents. Previous studies show that rofecoxib, a selective cyclooxygenase-2 inhibitor, protects against kainate-induced hippocampal cell death 3 days after seizures. Our aim was to determine whether rofecoxib attenuates visuospatial learning deficits and late neuronal death after kainate-induced seizures. Seizures were induced in Sprague-Dawley rats with kainic acid (10 mg/kg, i.p.). Eight hours later, animals received rofecoxib (10 mg/kg; n = 15) or vehicle (dimethylsulfoxide, n = 11). Animals were then treated daily for additional 2 or 9 days. Visuospatial learning was assessed in the Morris water maze (MWM) on days 5-9 after seizures. Seizure animals learned the MWM task significantly slower than non-seizure controls, but seizure animals showed higher swim speed (P < 0.05). Seizure animals receiving rofecoxib for 2 days showed no significant improvement in acquisition of the task compared to the vehicle group, even though mean latencies in the rofecoxib group were shorter from the third trial day onwards. This tendency was lost when rofecoxib was given for 9 days. TdT-mediated dUTP nick end labelling showed cell death in limbic structures 9 days after seizures. The time course of kainate-induced hippocampal cell death might be delayed by rofecoxib treatment, as the attenuation of cell death observed 3 days after seizures was no longer present after 9 days. We conclude that even though increasing evidence points to an injurious role of cyclooxygenase-2 products in acute brain injury processes, rofecoxib treatment failed to attenuate seizure-induced visuospatial learning deficits and the late phase of hippocampal neurodegeneration.

Animals↗
PubMed2003

Orexin-A (hypocretin-1) impairs Morris water maze performance and CA1-Schaffer collateral long-term potentiation in rats.

Glucose-sensitive neurons in the lateral hypothalamic area produce orexin-A (hypocretin-1) and orexin-B (hypocretin-2) and send their axons to the hippocampus, which predominantly expresses orexin receptor 1 showing a higher sensitivity to orexin-A. The purpose of the present study was to assess the effects of orexin-A on the performance of Wistar rats during the Morris water maze test and then to determine the effects of orexin-A on both the long-term potentiation and long-term depression in Schaffer collateral/commissural-CA1 synapses in hippocampal slices. The results of the Morris water maze test show that 1.0 and 10 nmol of orexin-A, when administered intracerebroventricularly, retarded spatial learning. A probe test examined after training of water maze task also showed an impairment in spatial memory. The results of an electrophysiological study using hippocampal slices demonstrated that 1.0 to 30 nM of orexin-A applied to the perfusate produces a dose-dependent and time dependent suppression of the long-term potentiation. In addition, the long-term depression was not affected by orexin-A. The results of a paired-pulse facilitation experiment indicated that the effects of orexin-A were post-synaptic and not due to presynaptic transmitter release. These results show that orexin-A impairs spatial performance and these impairments can be attributed to a suppression of long-term potentiation in the Schaffer collateral-CA1 hippocampal synapses.

Animals↗
PubMed1982

Sex differences in a children's spatial serial-learning task.

Boys (n = 80) and girls (n = 80) aged 9 to 10 completed a spatial-span test and a spatial serial-learning task. Corsi's block-tapping test was used for both. Sex differences were found on each: males performed better in both cases. The better performance of males on the spatial serial-learning task was independent of their superiority in the spatial-span test.

Child↗
PubMed1992

Effects of tetrahydroaminoacridine on spatial navigation of nucleus-basalis- and frontal-cortex-lesioned rats.

The present study investigates the effects of tetrahydroaminoacridine (THA: 1 and 3 mg/kg) on water maze (WM) spatial learning performance of intact, nucleus-basalis- (NB) lesioned, frontal-cortex- (FR) lesioned, or NB + FR-lesioned rats. NB lesions did not impair WM learning and had no effect on the WM performance deficit in FR-lesioned rats. THA at 1 or 3 mg/kg did not improve WM spatial memory of intact, NB-, FR-, or NB + FR-lesioned rats. These results suggest that 1) the cholinergic NB system is not a prerequisite for frontally mediated acquisition of WM performance, 2) THA treatment does not enhance spatial memory, and 3) THA is not effective in alleviating cognitive deficits induced by degeneration of the frontal cortex.

Animals↗
PubMed1992

Impaired acquisition of the Morris water maze following global ischemic damage in the gerbil.

Five minutes of global ischemia in the Mongolian gerbil impaired acquisition of a Morris water maze task when testing began 72 h after surgery. In spite of extensive damage to CA1 pyramidal cells, ischemic animals eventually learned to locate a submerged platform and performed normally on a subsequent retention test. Animals that were allowed a more protracted recovery period (21 days) acquired the task as readily as control gerbils. These results suggest that undamaged structures within and external to the hippocampal formation allow spatial learning to proceed at a somewhat reduced rate.

Animals↗
PubMed2005

Different rankings of inbred mouse strains on the Morris maze and a refined 4-arm water escape task.

The submerged platform or Morris water escape task is widely used to study genetic variation in spatial learning and memory, but interpretation is sometimes difficult because of wall hugging, jumping off the platform, floating or non-spatial swim strategies. We modified the task by introducing four wide arms into the circular tank and adding features that reduced, eliminated, or compensated for several competing behaviors. Three versions of the 4-arm task were evaluated in detail, and the third version yielded good results for six of eight inbred strains. Furthermore, the 4-arm task could be scored adequately without computerized video tracking. Although performance on the 4-arm task was generally superior to the Morris maze, the extent of the improvement was strain dependent. Two strains with retinal degeneration (C3H/HeJ, FVB/NJ) performed poorly on both the Morris and 4-arm mazes, whereas C57BL/6J and DBA/2J did well on both mazes. A/J performed poorly on the Morris task but became very proficient on the 4-arm maze, despite its strong tendency to hug the walls of the tank. The BALB/cByJ strain, on the other hand, exhibited the best probe trial performance on the Morris maze but was very slow in acquiring the 4-arm task. We conclude that no single task can reveal the full richness of spatially guided behavior in a wide range of mouse genotypes.

Analysis of Variance↗
PubMed1991

Effect of Org2766, an ACTH(4-9) analogue, on recovery after bilateral transection of the fimbria fornix in the rat.

Facilitation of recovery after peripheral or central damage of the nervous system induced by neuropeptides was recently extensively reported. In a previous study we reported that Org2766, an ACTH(4-9) analogue, enhances recovery as assessed in a spatial orientation task after unilateral transection of the fimbria fornix in the rat. It was suggested that cross-lateral compensation by the intact fimbria fornix hippocampal system could account for the peptide-induced recovery. Therefore, the facilitatory effect of this neuropeptide was investigated in the present study after bilateral transection of the fimbria fornix. The present results indicate that Org2766 also attenuated the behavioral deficit of bilaterally transected animals in a spatial learning task, but does not affect behaviour of the lesioned animals in a passive avoidance test.

Adrenocorticotropic Hormone↗
PubMed2002

Navigation in the Morris swim task as a baseline for drug discrimination: a demonstration with morphine.

A morphine versus saline discrimination was demonstrated using the Morris swim task as the behavioral baseline. The apparatus was a large circular pool filled with water made opaque by floating polypropylene pellets. Rats were placed in the tank in randomly selected locations (12 trials per session) and could escape by swimming to a platform submerged 2 cm below the surface. Morphine (5.6 mg/kg) or saline was injected prior to training sessions. The position of the platform in a given session depended on the drug condition, thus forming the basis for discriminative responding. Three of the 4 rats acquired the discrimination, as evidenced by direct swims to the condition-appropriate platform. Generalization probe sessions were conducted following acquisition. Probe sessions were preceded by injections of morphine (0, 1.0, 3.0, 5.6, or 10.0 mg/kg) and involved placing the rat in the pool for 1 min without a platform. Swim patterns revealed a gradient, with probe swimming more concentrated in the area of the morphine platform position after higher morphine doses. In addition, dose-dependent increases in the likelihood of swimming first to the morphine-associated platform location were obtained. These results illustrate the generality of drug discrimination across different behavioral procedures, and of particular interest with respect to spatial learning, demonstrate interoceptive stimulus control of navigation.

Animals↗
PubMed1999

Different effects of unilateral and bilateral hippocampal lesions in rats on the performance of radial maze and odor-paired associate tasks.

The hippocampus plays an important role in the declarative or explicit memory in humans and is necessary for allocentric spatial learning and olfactory memory in animals. In primates and rodents, the bilateral hemispheres of the brain (especially the forebrain) symmetrically and asymmetrically contribute to diverse cognitive manipulations. In this study, we investigated the role of the hippocampus in spatial memory and in odor-paired associate memory by unilaterally or bilaterally lesioning this region in rats. The bilateral removal, but not the unilateral removal, of the hippocampus impaired both the acquisition of spatial working memory in the radial maze task and the retrieval of maze performance tested 1 month after the acquisition trials. In contrast, neither bilateral nor unilateral removal impaired the odor-paired associate learning. These findings suggest that the hippocampus is critical to the spatial memory, and that a unilateral hippocampus is sufficient for executing a spatial task. The present results also indicate that the hippocampus plays a minor role in odor-dominated associate learning and that some kinds of memories in rats may be processed independently by the left or right hippocampus.

Animals↗
PubMed2005

Profound but transient deficits in learning and memory after global ischemia using a novel water maze test.

The pyramidal CA1 neurons of the hippocampus are critically involved in spatial learning and memory. These neurons are especially vulnerable to cerebral ischemia, but in spite of this, it has been consistently difficult to show any learning and memory deficits in two-vessel occlusion models of global ischemia. Transient global ischemia was induced in adult male rats under general anaesthesia administered by artificial respiration to prevent respiratory arrest. Systemic blood pressure was reduced to below 50 mmHg by instant adjustments of the halothane concentration, before and during bilateral occlusion of the carotid arteries. Cerebral blood flow was monitored by laser-Doppler flowmetry. Dying neurons were detected by TUNEL at 14 days after ischemia and surviving neurons by NeuN at 14 and 125 days after ischemia. Learning and memory was assessed in a novel water maze with three successive left-right choices. Transient global ischemia produced a profound and selective degeneration of CA1 neurons at 14 days after ischemia. This degeneration was associated with severe impairments in learning at 13 days after ischemia and in memory, as tested 24 h afterwards. At 125 days after ischemia, there was no significant learning and memory impairment, whereas the number of CA1 neurons was increased. These results show that transient global ischemia induced by two-vessel occlusion may lead to severe, but transient, impairments in learning and memory using a novel water maze, and that restored learning and memory is associated with an increased number of CA1 neurons.

Analysis of Variance↗
PubMed1996

Effects of ovariectomy upon performance of a maze learning paradigm in the adult female rat.

To determine what effect ovariectomy and the accompanying sudden loss of circulating gonadal hormones has on spatial learning performance in the adult rat, two groups of rats were tested on the Lashley III simple alley maze following surgery. Ovariectomized animals were compared with a control group of animals that underwent laparotomy at the same time. The ovariectomized group evidenced superior performance on the maze task, as measured by latency to reach goal (running times) and error scores. It is suggested that this finding provides further evidence for the role of gonadal steroid hormones in the manipulation of functions related to learning and memory, especially in the hippocampus.

Animals↗
PubMed2005

Stress-induced changes in spatial memory are sexually differentiated and vary across the lifespan.

Stress exposure, depending on intensity and duration, elicits adaptive or maladaptive physiological changes. The same general pattern of advantageous versus deleterious stress effects appears to exist for some cognitive functions, particularly spatial learning and memory performance. This article reviews sex differences in response to stress on a variety of spatial tasks. In general, females are more resistant than males to stress-induced impairments on spatial tasks, including the radial arm maze and object placement. In young adulthood, chronic stress (restraint, 6 h per day for 21 days) impairs male performance on both tasks but leads to behavioural enhancements in females. Furthermore, these sex-dependent stress effects are influenced by both organisational and activational oestrogenic effects. Additionally, sex-specific stress responses vary depending on developmental age at the time of stress exposure. Male behavioural stress responses appear fixed across the lifespan (i.e. stress-induced cognitive impairments) whereas female stress responses appear more variable (i.e. stress-induced enhancements observed in young adulthood are different in response to prenatal stress and diminished following stress exposure at old age). These findings underscore the point that many effects obtained in males cannot be generalised to females and highlight the need to investigate the stress response at different ages and in both sexes.

Adaptation, Physiological↗
PubMed1998

Amygdalar NMDA receptors are critical for new fear learning in previously fear-conditioned rats.

NMDA receptors in the amygdala seem to be critical for fear conditioning in naive rats. Recent spatial-learning studies suggest that previous learning protected animals from the amnesic effect of NMDA antagonists on new learning (of a similar behavioral task). Therefore, the present study examined whether blocking of NMDA receptors in the basolateral nucleus of the amygdala (BLA) prevents new fear learning in previously fear-conditioned rats, as measured by freezing behavior. Intra-BLA infusions of the NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (APV) completely blocked fear conditioning to a tone stimulus in animals that had previously been fear-conditioned to a light stimulus. Similar results were obtained with intra-BLA infusions of APV before contextual fear conditioning in rats that had been fear-conditioned to a different context. Additional experiments showed that intra-BLA APV infusions substantially interfere with the expression and extinction of conditioned fear to tone, light, and context stimuli. Together, these results indicate that NMDA receptors in the BLA are crucial for the encoding of new fear memories (i.e., the formation of specific conditioned stimulus-unconditioned stimulus association), the expression of conditioned fear responses, and the extinction of acquired fear.

Acoustic Stimulation↗
PubMed2001

The effects of lesions to the rat hippocampus or rhinal cortex on olfactory and spatial memory: retrograde and anterograde findings.

The role of the hippocampal system in retrograde and anterograde amnesia was investigated by using a novel olfactory-guided paradigm and a traditional test of spatial learning. In the retrograde study, rats were trained on a sequence of two-choice olfactory discriminations in the weeks prior to receiving neurotoxic lesions of the hippocampus or aspiration lesions of the perirhinal-entorhinal cortex. Memory tests for preoperatively learned discriminations revealed no statistical impairment for subjects with damage to the hippocampus on a problem learned remote in time from surgery (i.e., 4 weeks +) or on the two recently learned discriminations (i.e., 1-3 weeks prior to surgery). The performance of subjects with perirhinal-entorhinal damage provided an important comparison for subjects with specific hippocampal lesions. Despite showing intact memory for the remotely learned problem, perirhinal-entorhinal damage resulted in numerically (although not significantly) weaker performance on postoperative tests of retention for the discriminations learned in the 3 weeks prior to surgery. In the anterograde portion of the study, long-term memory for newly acquired discriminations was spared in subjects with damage to the hippocampus, whereas subjects in the perirhinal-entorhinal lesion group again showed the weakest memory performance on these tests of 5-day retention. Postoperative water maze learning was uniformly impaired in subjects with damage to the hippocampus and perirhinal-entorhinal cortex, thus confirming the effect of these lesions and supporting the involvement of these brain areas in spatial processes. These findings further dissociate the specific involvement of the hippocampus in tasks of a spatial-relational nature versus nonrelational tasks, such as discrimination learning and recognition memory (e.g., Duva et al., 1997; Eichenbaum, 1997; Eichenbaum, Schoenbaum, Young, & Bunsey, 1996). Moreover, the results suggest that damage to the hippocampus itself does not contribute to retrograde or anterograde memory impairments for all types of information, whereas the data suggest a more important role for the perirhinal-entorhinal cortex in recognition memory, irrespective of modality.

Animals↗
PubMed2003

Environmental enrichment reverses cognitive and molecular deficits induced by developmental lead exposure.

Long-term deficits in cognitive function are the principal effects of lead (Pb2+) exposure in children and can be modeled in experimental animals. Current therapeutic approaches in the treatment of childhood Pb2+ intoxication are not effective in reversing learning deficits once they have occurred. We report that environmental enrichment reverses long-term deficits in spatial learning produced by developmental Pb2+ exposure in rats. Enhanced learning performance of Pb2+-exposed animals reared in an enriched environment was associated with recovery of deficits in N-methyl-D-aspartate receptor subunit 1 (NR1) mRNA and induction of brain-derived neurotrophic factor (BDNF) mRNA in the hippocampus. The effect of environmental enrichment on NR1 and BDNF gene expression was specific to Pb2+-exposed animals and was present in the absence of changes in the NR2B subunit of the N-methyl-D-aspartate receptor, GluR1, alpha CamKII, or PSD-95 gene expression measured in the same animals. Our findings demonstrate that the learning impairments and NR1 subunit mRNA deficits resulting from developmental Pb2+ exposure are reversible if the animals are provided with an enriched environment even after the exposure has occurred. We propose environmental enrichment as a basis for the treatment of childhood Pb2+ intoxication.

Age Factors↗