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PubMed1994

Naloxone facilitates spatial learning in a water-maze task in female, but not male, adult nonbreeding meadow voles.

The present study examined the effects of the opiate antagonist naloxone on spatial acquisition and retention in a water-maze task by adult, nonbreeding, male and female meadow voles (Microtus pennsylvanicus). Voles were required to learn the position of a hidden, submerged platform using distal visual cues. There were four trials per day for 6 days. Daily pretraining (15 min before first trial) systemic administrations of naloxone (1.0 mg/kg, IP) significantly facilitated spatial acquisition in female, but not in male, voles in a water-maze task on days 2, 3, and 4. There were two probe tasks given 1 day and 1 week after the last training trial. All groups acquired the spatial task by the end of the fifth day with no significant effects of naloxone on retention of the spatial task. There were also no significant sex differences in acquisition of the spatial task and task retention in control, nonbreeding adult voles. It is suggested that the lack of sex differences in basal spatial performance may be related to the low levels of testosterone in male nonbreeding voles. The obtained sex differences in the effects of naloxone on spatial acquisition are considered in relation to sex differences in stress, opiate responses, and gonadal steroid levels.

Animals↗
PubMed1997

Comparison of effects of global cerebral ischaemia on spatial learning in the standard and radial water maze: relationship of hippocampal damage to performance.

Groups of rats which had undergone global ischaemia for 10, 15 or 20 min using the four-vessel occlusion technique were compared with sham-operated controls on learning to locate a submerged platform in both acquisition and working memory tasks in a standard Morris water maze, and in a working memory task in an eight-channel water radial maze. Ischaemic rats showed duration-related impairments in all three tasks. The water radial maze task was learned more slowly than standard water maze tasks, but deficits were long-lasting. In the first phase of training in the radial water maze controls were more reluctant than ischaemic rats to visit all arms of the maze, and were subsequently found to spend less time on the open arms of an elevated plus-maze. However, differences in anxiety are not likely to account for differences in working memory performance in the radial water maze, as groups showed similar error rates before and after habituation to the maze. Histological examination showed that cell loss occurred chiefly in the CA1 field of the hippocampus and was linearly related to duration of occlusion. Cell loss was significantly correlated with the extent of impairment, but the pattern of relationships varied across the different tasks. For water maze acquisition, deficits in latency, heading angle and time spent in the training quadrant related more strongly to CA1 than CA3 cell loss, but radial water maze impairments showed the reverse tendency. In all cases correlations were substantially reduced following exclusion of rats with maximal CA1 cell loss, although a modest relationship with CA1 damage remained for latency in acquisition and working memory tasks, and heading angle on the probe trial. These results suggested that relationships between water maze impairments and cell loss are robust only after near total destruction of the dorsal CA1 field.

Animals↗
PubMed2000

Antisense DNA against calcineurin facilitates memory in contextual fear conditioning by lowering the threshold for hippocampal long-term potentiation induction.

In the previous study, we demonstrated that the antisense oligodeoxynucleotides against calcineurin Aalpha and Abeta, catalytic subunits of Ca(2+)/calmodulin-dependent protein phosphatase, produce a facilitatory effect on long-term potentiation induction in the hippocampal CA1 region in rats anesthetized with urethane. Here, we have studied how animals, in which the hippocampal long-term potentiation induction is enhanced by antisense oligodeoxynucleotides against calcineurin, perform in learning tasks that depend on hippocampal function. The rats received antisense oligodeoxynucleotides by bilateral ventricular administration via miniosmotic pumps. We tested four groups of rats, three infused with either antisense oligodeoxynucleotides, scramble oligodeoxynucleotides, or saline, and untreated rats, for two types of hippocampus-dependent learning, water maze and contextual fear conditioning. After the behavioral tests, we conducted a long-term potentiation induction test to determine whether long-term potentiation induction was enhanced. In contextual fear conditioning, rats in which long-term potentiation induction was enhanced by antisense oligodeoxynucleotides displayed significantly more conditioned freezing response than control rats. Rats with enhanced long-term potentiation induction showed no differences in shock sensitivity, general activity, or light-dark choice from control rats. In contrast with contextual fear conditioning, rats with enhanced long-term potentiation induction showed no difference in spatial learning performance on the water maze compared with control rats. These results demonstrate that an enhancement in long-term potentiation induction produced by the inhibition of calcineurin leads to an increase in memory strength in specific forms of hippocampus-dependent learning.

Animals↗
PubMed1991

Impaired tunnel-maze behavior in rats with sensory lesions: vestibular and auditory systems.

Maze behavior of rodents provides insight into processes of learning and memory and also serves to assess cognitive functions in neurotoxicity tests. Neurotoxic agents may impair maze behavior by acting upon different parts of the nervous system. To assess the dependence of maze learning upon vestibular and/or auditory input, the two systems were lesioned. Daily treatment of rat pups with streptomycin (400 mg/kg sc) on postnatal day 11 to 22 caused irreversible impairment of vestibular and auditory functions, whereas, 20 injections of neomycin in adult rats (100 mg/kg sc, postnatal weeks 8 to 11) led to hearing loss only. Hearing loss was assessed by absence of Preyer's reflex and impaired vestibular function by loss or shortened duration of postrotatory nystagmus. Learning in the unbaited 6-arm radial maze was tested at the age of 2 to 3 mon using a maze configuration that allowed to assess order of arm entries ("working memory") and left-right discrimination within each arm ("reference memory"). Treatment with streptomycin but not with neomycin led to impaired order of arm entries. Since treatment with streptomycin failed to induce any signs of brain lesions, impaired maze learning is considered to result from destruction of vestibular hair cell receptors with subsequent vestibular impairment and not from hearing loss or cognitive impairment.

Animals↗
PubMed2002

Animal model of dementia induced by entorhinal synaptic damage and partial restoration of cognitive deficits by BDNF and carnitine.

A rat dementia model with cognitive deficits was generated by synapse-specific lesions using botulinum neurotoxin (BoNTx) type B in the entorhinal cortex. To detect cognitive deficits, different tasks were needed depending upon the age of the model animals. Impaired learning and memory with lesions were observed in adult rats using the Hebb-Williams maze, AKON-1 maze and a continuous alternation task in T-maze. Cognitive deficits in lesioned aged rats were detected by a continuous alternation and delayed non-matching-to-sample tasks in T-maze. Adenovirus-mediated BDNF gene expression enhanced neuronal plasticity, as revealed by behavioral tests and LTP formation. Chronic administration of carnitine over time pre- and post-lesions seemed to partially ameliorate the cognitive deficits caused by the synaptic lesion. The carnitine-accelerated recovery from synaptic damage was observed by electron microscopy. These results demonstrate that the BoNTx-lesioned rat can be used as a model for dementia and that cognitive deficits can be alleviated in part by BDNF gene transfer or carnitine administration.

Aging↗
PubMed1998

The immune system can affect learning: chronic immune complex disease in a rat model.

Evidence is presented that the immune system can affect central nervous system functioning, leading to changes in learning. Immune complex disease is induced in rats and their behavior tested using a Lashley maze. Significant differences in behavior were found between the animals with high disease activity and those with low disease activity and the non-disease controls. These changes were not due to uremia and are most likely due to the immune response. There is some evidence immune complex deposits in the choroid plexus may play some role, but not the sole or major role in the behavioral changes. This provides a model by which immunologic processes can cause neuropsychiatric manifestations in autoimmune diseases like lupus, as well as showing that immune processes can affect behavioral functioning.

Animals↗
PubMedDate not supplied

Glucose treatment attenuates spatial learning and memory deficits of aged rats on tests of hippocampal function.

Groups of old and young rats were administered three tests of spatial learning and memory that are known to be sensitive to hippocampal dysfunction: the radial arm maze (RAM), spatial non-matching-to-sample (SNMTS), and a spatial vs. local cue-preference task. Old rats performed worse than young rats on the RAM and SNMTS tasks; on the cue-preference task, young rats were biased to use spatial cues, whereas old rats exhibited strong preferences for distinct, local cues. Peripheral injections of glucose (100 mg/kg) improved performance by old rats on the RAM and SNMTS, which correlated with measures of glucose metabolism. Glucose treatment did not affect old rats performance on the cue-preference task. There was evidence that glucose-treatment improved performance of young rats in the RAM test, but not the other tests. The results extend the range of tasks on which glucose-induced cognitive enhancement has been demonstrated in aged rats, and provides further evidence that memory loss resulting from hippocampal dysfunction is especially amenable to glucose treatment.

Aging↗
PubMed2004

Intramaze and extramaze cue processing in adult APPSWE Tg2576 transgenic mice.

The present study examined spatial and nonspatial learning in adult Tg2576 mice. Transgenic mice were impaired in acquisition of a T-maze forced-choice alternation task. However, mutant mice were as sensitive as control mice to the introduction of retention intervals and proactive interference, and this suggested that short-term memory processes were intact in Tg2576 mice. Probe trials revealed that the Tg2576 mice did not use an allocentric strategy to navigate to the goal arm. However, mutant mice acquired an intramaze brightness discrimination, a simple room discrimination, and a contextual biconditional left-right discrimination in a T maze. Results suggest that Tg2576 mice are able to process both intramaze and extramaze stimuli but are impaired in forming an allocentric representation of their environment.

Amyloid beta-Protein Precursor↗
PubMedDate not supplied

Overexpression of a calcium-binding protein, S100 beta, in astrocytes alters synaptic plasticity and impairs spatial learning in transgenic mice.

Recent evidence suggests that slowly propagating Ca2+ waves from astrocytes can modulate the function of neurons. Altering astrocytic calcium processes in vivo may therefore affect neuronal and behavioral phenotypes. Previously, we generated transgenic mice that overexpress an astrocytic calcium-binding protein, S100 beta. Immunocytochemistry and in situ hybridization showed elevated expression in the astrocytes of the hippocampus and other brain regions. Neurons in the hippocampus were negative for S100 beta. In this paper we analyze the hippocampal electrophysiology and learning properties of mice from two transgenic lines. Significant differences were found between the hippocampal slices of normal and transgenic mice in their response to high frequency (100 Hz) stimulation. The overall distribution of post-tetanic excitatory postsynaptic potentials (EPSP) of the slices from the transgenic mice was shifted significantly toward smaller values to a degree that 25% of slices exhibited depression. The altered hippocampal neurophysiology was accompanied by an impairment in a hippocampal-dependent learning task. Transgenic mice showed significant impairment in a spatial version of the Morris water maze, however, they performed normally in non-spatial tasks. Probe trials showed that transgenic mice, though significantly impaired, also acquired spatial information. The results suggested that the impairment was not due to motor dysfunction, impaired vision or motivation of the transgenic mice, findings compatible with a possible hippocampal mechanism. We conclude that overexpression of S100 beta in astrocytes impairs, but does not abolish, the ability to solve a spatial task, and it leads to a significantly decreased post-tetanic potentiation in the hippocampal slice. We hypothesize that the changes are due to calcium mediated processes. Our results support the notion that astrocytes are involved in higher brain functions.

Animals↗
PubMed2005

Estradiol to aged female or male mice improves learning in inhibitory avoidance and water maze tasks.

Although 17beta-Estradiol (E2) improves cognitive performance of aged female mice, its mnemonic effects when administered post-training to aged male mice have not been examined. E2 (10 microg, SC) or oil vehicle was administered to intact, 24-month-old female or male congenic (primarily C57BL/6 background) mice immediately after training in the inhibitory avoidance or water maze tasks. Following behavioral testing, effects of 1 or 24 h of E2 exposure on hippocampal levels of E2 and brain-derived neurotrophic factor (BDNF) were examined. Female and male mice administered E2 showed significantly better performance in the inhibitory avoidance task than did vehicle-administered mice. When tested 24 h after training, mice that received E2 had significantly longer latencies to cross-over to the shock-associated side of the chamber than did vehicle-administered mice. Female or male mice administered E2 showed significantly better performance in the reference memory aspect of the spatial water maze task. When tested 30 min after training, mice administered E2 had shorter latencies to, and spent longer swimming in, the quadrant that the hidden platform had previously been located in. E2 administration produced physiological levels of E2 in the hippocampus 1 and 24 h after E2. BDNF levels in the hippocampus were decreased following 1 h of E2 exposure compared to vehicle. These findings suggest that E2 to female and male mice may overcome age-related deficits in reference memory in an emotional or spatial learning task.

Aging↗
PubMed2005

Long-term impaired memory following predatory stress in mice.

Brief exposure of mice to unavoidable predatory stimuli is associated with behavioral and neurochemical changes consistent with increased anxiety and produces short-term impaired learning restored by acute fluoxetine treatment, but not by diazepam. The present study investigated long-lasting changes induced by a unique unavoidable cat exposure in BALB/c mice on learning abilities using learning tests (radial maze, spatial configuration of objects recognition test). Results from the group comparison showed that predatory exposure induced significant learning disabilities in the radial maze (16 to 22 days poststressor) and in the spatial configuration of objects recognition test (26 to 28 days poststressor). These findings indicate that memory impairments may persist for extended periods beyond a predatory stress. This animal model of unique exposure of mice to unavoidable predatory stimuli has proven to be a useful model for the study of reactions to traumatic stress.

Animals↗
PubMed1999

Spatial learning and performance in the radial arm maze is impaired after N-methyl-D-aspartate (NMDA) receptor blockade in striatal subregions.

These experiments addressed the role of striatal N-methyl-D-aspartate (NMDA) receptors in spatial behavior in the radial arm maze. Rats treated with the NMDA antagonist D-2-amino-5-phosphonopentanoic acid (AP-5) in the nucleus accumbens core, medial caudate, and posterior caudate were all significantly impaired in acquiring the correct spatial responses. In contrast, rats infused with AP-5 in the nucleus accumbens shell showed little impairment. When rats in all groups had learned the maze and were performing at similar levels, AP-5 had relatively little effect except in the posterior caudate group, where errors and trial times were again increased. These findings demonstrate the importance of NMDA receptor-dependent activity within the accumbens and caudate in spatial learning and performance. The neural processes necessary for adaptive spatial learning in complex environments may recruit multiple cortical systems having specialized functions, which in turn are integrated in widespread striatal regions.

2-Amino-5-phosphonovalerate↗
PubMed2004

Hippocampal damage in mouse and human forms of systemic autoimmune disease.

Systemic lupus erythematosus (SLE) is frequently accompanied by neuropsychiatric (NP) and cognitive deficits of unknown etiology. By using autoimmune MRL-lpr mice as an animal model of NP-SLE, we examine the relationship between autoimmunity, hippocampal damage, and behavioral dysfunction. Fluoro Jade B (FJB) staining and anti-ubiquitin (anti-Ub) immunocytochemistry were used to assess neuronal damage in young (asymptomatic) and aged (diseased) mice, while spontaneous alternation behavior (SAB) was used to estimate the severity of hippocampal dysfunction. The causal relationship between autoimmunity and neuropathology was tested by prolonged administration of the immunosuppressive drug cyclophosphamide (CY). In comparison to congenic MRL +/+ controls, SAB acquisition rates and performance in the "reversal" trial were impaired in diseased MRL-lpr mice, suggesting limited use of the spatial learning strategy. FJB-positive neurons and anti-Ub particles were frequent in the CA3 region. Conversely, CY treatment attenuated the SAB deficit and overall FJB staining. Similarly to mouse brain, the hippocampus from a patient who died from NP-SLE showed reduced neuronal density in the CA3 region and dentate gyrus, as well as increased FJB positivity in these regions. Gliosis and neuronal loss were observed in the gray matter, and T lymphocytes and stromal calcifications were common in the choroid plexus. Taken together, these results suggest that systemic autoimmunity induces significant hippocampal damage, which may underlie affective and cognitive deficits in NP-SLE.

Aging↗
PubMed1995

Thiamine deficiency in rats produces cognitive and memory deficits on spatial tasks that correlate with tissue loss in diencephalon, cortex and white matter.

Exploratory activity, spontaneous alternation, learning and memory abilities were examined in the pyrithiamine-induced thiamine deficiency (PTD) rat model of Wernicke-Korsakoff's syndrome and pair-fed controls (CT). PTD and CT animals showed normal retention of a single trial of a passive avoidance task acquired prior to the acute stages of thiamine deficiency. While there were no significant group differences in spontaneous activity, PTD animals with extensive damage to internal medullary lamina (IML-lesioned) of thalamus and mammillary body nuclei demonstrated a significant decrease in spontaneous alternation and were significantly impaired in learning both the initial spatial non-matching-to-position (NMTP) task and the reverse MTP task. PTD animals without IML damage (IML-spared) were only impaired on the acquisition of NMTP. Examination of response patterns suggest that the learning impairment was related to an inability to adopt or shift to the appropriate response rule. Performance of PTD IML-lesioned animals on NMTP mixed-delay sessions (4, 30, 60, 90 s) was similar to controls and PTD IML-spared, but was significantly lower on MTP delay trials. These IML-lesioned rats also had significant reductions in thickness of frontal and parietal cortex, corpus callosum and severe neuronal loss in anterior and reticular thalamic nucleic. Four PTD IML-lesioned animals that were unable to learn the NMTP task had more extensive cortical, white matter and thalamic damage than the PTD IML-lesioned animals that did learn the task. These results demonstrate that thiamine deficiency in the rat produces behavioral changes ranging from mild cognitive deficits to severe learning and memory impairments. Pathologic damage following a bout of thiamine deficiency also varies from neuronal loss in select thalamic nuclei to tissue loss in large regions of thalamus, mammillary bodies and cortex. Learning and memory deficits are closely related to the degree of cortical and diencephalic damage.

Animals↗
PubMed2004

Septal infusions of glucose or pyruvate with muscimol impair spontaneous alternation.

This experiment examined the effects of co-infusing the GABA agonist muscimol (0.5 nmol) with 33 nmol of glucose, pyruvate, fructose or sorbitol into the medial septum on spontaneous alternation. Only co-infusions of muscimol with glucose or pyruvate impaired spontaneous alternation performance; none of the other infusions had any significant effects. The findings suggest that glucose metabolism rather than hyperosmolarity is involved in the memory-impairing interaction between glucose and muscimol.

Animals↗
PubMed2006

Intracellular Abeta and cognitive deficits precede beta-amyloid deposition in transgenic arcAbeta mice.

The brain pathology of Alzheimer's disease is characterized by abnormally aggregated Abeta in extracellular beta-amyloid plaques and along blood vessel walls, but the relation to intracellular Abeta remains unclear. To address the role of intracellular Abeta deposition in vivo, we expressed human APP with the combined Swedish and Arctic mutations in mice (arcAbeta mice). Intracellular punctate deposits of Abeta occurred concomitantly with robust cognitive impairments at the age of 6 months before the onset of beta-amyloid plaque formation and cerebral beta-amyloid angiopathy. beta-Amyloid plaques from arcAbeta mice had distinct dense-core morphologies with blood vessels appearing as seeding origins, suggesting reduced clearance of Abeta across blood vessels in arcAbeta mice. The co-incidence of intracellular Abeta deposits with behavioral deficits support an early role of intracellular Abeta in the pathophysiological cascade leading to beta-amyloid formation and functional impairment.

Age Factors↗
PubMed2004

Age-related vulnerability to diencephalic amnesia produced by thiamine deficiency: the role of time of insult.

Age is a risk factor for the development of many neurological disorders, including alcohol-related neurological disorders. A rodent model of Wernicke-Korsakoff Syndrome (WKS), acute pyrithiamine-induced thiamine deficiency (PTD), produces diencephalic damage and impairments of memory similar to what is seen in WKS patients. Advanced age increases the vulnerability to the cascade of acute and some chronic neurological events caused by PTD treatment. Interactions between PTD treatment and age at the time of treatment (3, 10, or 21 months), in addition to the effects of an increased recovery period, were examined relative to spatial memory impairment and neuropathology in Fischer 344 rats. Although acute neurological disturbances and medial thalamic brain lesions were more prevalent in middle-aged and senescent rats exposed to PTD treatment, relative to young rats, behavioral data did not support the view that PTD and aging have synergistic effects. In addition, both advanced age and PTD treatment result in a loss of basal forebrain cholinergic neurons, though there was no interaction. Despite the fact that no convincing evidence was found for an effect of extended recovery time on neuropathology measures, young rats given an extensive recovery period displayed less working memory impairment. In summary, these data provide evidence for an increased susceptibility of the aged rat to the acute neurological consequences and diencephalic pathology associated with PTD treatment and indicated a similar vulnerability of the middle-aged rat. However, the synergistic interaction between aging and PTD treatment in thalamic tissue loss did not express behaviorally.

Aging↗