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At least 1,135 records · Page 63Linked to original sources
PubMed2004

Apoptotic neurodegeneration induced by ethanol in neonatal mice is associated with profound learning/memory deficits in juveniles followed by progressive functional recovery in adults.

Administration of ethanol to rodents during the synaptogenesis period induces extensive apoptotic neurodegeneration in the developing brain. This neurotoxicity may explain the reduced brain mass and neurobehavioral disturbances in human Fetal Alcohol Syndrome (FAS). Here, we report binge-like exposure of infant mice to ethanol on a single postnatal day triggered apoptotic death of neurons from diencephalic structures that comprise an extended hippocampal circuit important for spatial learning and memory. The ethanol exposure paradigm yielding these neuronal losses caused profound impairments in spatial learning and memory at 1 month of age. This impairment was significantly attenuated during subsequent development, indicating recovery of function. Recovery was not associated with increased neurogenesis, suggesting plastic reorganization of neuronal networks compensated for early neuronal losses. We hypothesize that neuroapoptotic damage in homologous regions of human brain underlies cognitive deficits in FAS and the human brain of FAS victims has a similar capacity to effect functional recovery.

Animals↗
PubMed2004

Pharmacological manipulation of mGlu2 receptors influences cognitive performance in the rodent.

Atrophy of the medial temporal lobes, including the glutamatergic cortical-hippocampal circuitry, is an early event in Alzheimer's disease (AD) and probably contributes to the characteristic short-term mnemonic decline. Pharmacological strategies directly targeted to ameliorating this functional decline may represent a novel approach for the symptomatic treatment of AD. Presynaptic group II metabotropic glutamate receptors (i.e. mGlu2 and mGlu3) exert a powerful modulatory influence on the function of these pathways, in particular the perforant pathway. Using a combination of mGlu2 receptor knockout mice and the group II agonist LY354740, we show that activation of mGlu2 receptors produces a cognitive impairment, i.e. a delay-dependent deficit in delayed matching and non-matching to position, and impaired spatial learning in a Morris water maze. Conversely, a group II antagonist, LY341495, improved acquisition of spatial learning. LY354740 potently reduced field excitatory postsynaptic potentials in hippocampal slices from wild type but not mGlu2 receptor knockout mice. Taken together, these results suggest that activation of mGlu2 receptors evokes a powerful inhibitory effect on hippocampal synaptic transmission and mGlu2 agonists produce a cognitive deficit consistent with this change. Conversely, mGlu2 receptor antagonists may improve certain aspects of cognition and thus represent a novel approach for the symptomatic treatment of AD.

Amino Acids↗
PubMed2002

Nociceptin/orphanin FQ modulation of ionic conductances in rat basal forebrain neurons.

Nociceptin/orphanin FQ (N/OFQ) is an endogenous opioid-like heptadecapeptide that plays an important role in a variety of physiological functions. N/OFQ and its receptor opioid receptor-like orphan receptor-1 are abundant in the diagonal band of Broca (DBB), a basal forebrain nucleus where the loss of cholinergic neurons is linked to memory and spatial learning deficits. In the whole animal, central injections of N/OFQ have been shown to disrupt spatial learning. In this study, we investigated the basis for these behavioral observations by examining the cellular effects of N/OFQ on chemically identified DBB neurons. Whole cell patch-clamp recordings were performed on enzymatically dissociated DBB neurons. Under voltage-clamp conditions, bath application of N/OFQ (10 pM-1 microM) resulted in a dose-dependent depression of whole cell currents. Single cell reverse transcription-polymerase chain reaction analysis identified cholinergic and fewer GABAergic cells to be N/OFQ-responsive. [Nphe(1)]nociceptin-(1-13)-NH(2) and CompB (J-113397) antagonized the N/OFQ response, but both compounds also displayed partial agonist activity. Using a combination of channel blockers we determined that the effects of N/OFQ were mediated via a suite of Ca(2+) (N- and L-type) and Ca(2+)-dependent K(+) (iberiotoxin-sensitive) conductances. In addition, biophysical analysis of voltage subtraction protocols revealed that N/OFQ reduces transient outward and the delayed rectifier K(+) currents. Because N-type and L-type Ca(2+) channels are important in the context of neurotransmitter release, our observations indicate that N/OFQ inhibition of Ca(2+)-dependent conductances in cholinergic neurons would be expected to result in depression of acetylcholine release, which may explain the behavioral actions of N/OFQ in the brain.

Acetylcholine↗
PubMed1995

Spatial location learning in mice with ibotenate lesions of entorhinal cortex or subiculum.

This study examined the effects of ibotenate lesions of either the entorhinal cortex (EC) or the subiculum (SUB) on the ability of mice to memorize a single spatial location (initial discrimination), and on their capacity to switch to a new location (transfer) following the initial learning in an eight-arm radial maze. Results indicated that mice with ibotenate lesions of the EC or SUB were impaired in postoperative acquisition of the spatial discrimination task, making more reference, but not working memory, errors and displaying fewer first correct response trials than sham-operated control mice. Furthermore, additional damage to the ventral hippocampus exacerbated the impairment of performance induced by lesions of the SUB alone. In addition, all mice, except for the combined lesion group, exhibited similar performance levels when they were trained to choose another arm of the maze that had not previously been baited (transfer). These findings suggest that both the EC and the SUB play important roles in spatial information processing in mice.

Animals↗
PubMed1988

DBA/2Ibg mice are incapable of cholinergically-based learning in the Morris water task.

In comparison to C57BL/6Ibg mice, DBA/2Ibg mice are slow to find a submerged platform in the Morris water task. Spatial learning in this task is known to be severely disrupted by treatments that reduce muscarinic cholinergic function. DBA mice were chronically treated with diisopropylfluorophosphate (DFP) in order to decrease muscarinic binding in the brain. Despite significant losses of binding sites in cortex, midbrain, hindbrain, hippocampus, and striatum, the mice failed to show an effect of DFP treatment on latency to reach the platform. Saline-treated DBA mice showed only marginal preference for searching the appropriate region of the pool during a probe trial in which the platform was absent from the pool. The pattern of search behavior was not altered by DFP treatment. These data are in strong contrast to data obtained previously with C57BL/6Ibg mice, which show accurate search behavior that is completely disrupted by DFP treatment. DBA mice thus appear incapable of true, cholinergically-mediated spatial learning. It is hypothesized that these mice lack normal function of the septo-hippocampal system.

Animals↗
PubMedDate not supplied

Teaching old rats new tricks: age-related impairments in olfactory reversal learning.

Recent work suggests that normal aging may be associated with decline in different brain systems. In the present study, young and aged Long-Evans rats were tested in a spatial version of the Morris water maze dependent on medial temporal lobe function and also on an odor discrimination reversal task previously used to investigate orbitofrontal function. Aged rats acquired the odor discrimination problems normally but were impaired in acquiring subsequent reversals of the problems. A subset of the aged rats also exhibited impaired spatial learning in the water maze. There was no correlation between reversal performance and spatial learning in the aged rats, indicating that the reversal learning impairment was not related to decline in medial temporal lobe function. Instead the performance of the aged rats on the odor discrimination task resembled that of young rats with neurotoxic lesions of orbitofrontal cortex. These data indicate that rats show independent decline of different brain systems during normal aging and suggest orbitofrontal cortex as one prefrontal area where changes may be localized for further study.

Aging↗
PubMed2000

Sex differences, but no seasonal variations in the hippocampus of food-caching squirrels: a stereological study.

Recent studies have described sex differences in the relative size of the hippocampus that are associated with sex differences in space use in birds and short-lived mammals. A correlation between spatial learning and increased hippocampal volume has also been demonstrated in food-caching animals. Such results suggest that sexually dimorphic spatial learning (sex differences in space use during the breeding season) and seasonal variations in food-caching behavior (spatial memory for cache locations) might correlate with morphological changes in the hippocampus of adult long-lived mammals. We used modern stereological techniques to examine the volume and neuron number of the structures forming the hippocampal complex (dentate gyrus, CA3, and CA1) of wild adult eastern gray squirrels (Sciurus carolinensis) throughout the year. We observed differences in brain size between samples collected at different times of the year (October, January, and June). Our analysis showed sex differences, but no seasonal variations, in the volume of CA1 stratum oriens and stratum radiatum. There were no sex differences or seasonal variations in the relative volume or the number of neurons of any other layer of the structures forming the hippocampal complex. These results confirm the existence of sex differences in the structure of the hippocampus; however, this sexual dimorphism does not vary seasonally in adulthood and is likely to result from developmental processes. These results do not support the hypothesis that seasonal variations in food-caching behavior might correlate with morphological changes, such as variations in volume or neuron number, in the hippocampal complex of adult long-lived mammals.

Age Factors↗
PubMed2006

Insulin-like growth factor 1 reduces age-related disorders induced by prenatal stress in female rats.

Stress during the prenatal period can induce permanent abnormalities in adult life such as increased anxiety-like behavior and hyperactivity of hypothalamo-pituitary-adrenal (HPA) axis system. The present study was designed to investigate whether prenatal stress could induce spatial learning impairment in aged female rats. Furthermore, since it has been recently reported that insulin-like growth factor 1 (IGF-1) attenuates spatial learning deficits in aged rats and promotes neurogenesis in the hippocampus, we assessed the impact of a chronic infusion of IGF-1 on age-related disorders. Our results show that females stressed during prenatal life exhibit learning impairments in the water maze task. Chronic IGF-1 treatment restores their spatial abilities, reduces their HPA axis dysfunction and increases plasma estradiol levels. Parallel to these effects, chronic IGF-1 up-regulates neural proliferation in the dentate gyrus of the hippocampus. These findings support the hypothesis of an early programming of the vulnerability to some neurological diseases during senescence and reinforce the potential therapeutic interest of IGF-1 during brain aging.

Animals↗
PubMed1998

Molecular manipulations of extracellular superoxide dismutase: functional importance for learning.

Extracellular superoxide dismutase (EC-SOD) controls the availability of extracellular superoxide (O2.-), which is important for a variety of physiological pathways, including the primary means of inactivating nitric oxide (NO). The role of EC-SOD in neurobehavioral function has been until now unexplored. In the current studies, the phenotypic expression of genotypic alterations of EC-SOD production in mice were characterized for spatial learning and memory. Dramatic impairments in spatial learning in the win-shift 8-arm radial maze were seen in both EC-SOD knockout mice and EC-SOD overexpressing mice. The EC-SOD overexpressing mice were further characterized as having significant deficits in a repeated acquisition task in the radial-arm maze, which permitted the dissociation of long and short-term learning. Long-term learning was significantly impared by EC-SOD overexpression, whereas short-term learning was not significantly affected by EC-SOD overexpression. No systems have been shown to be importantly involved in learning and memory. This may be important in the current studies because EC-SOD has primary control over the inactivation of NO. We found that EC-SOD overexpressing mice were resistant to the cognitive effects of L-NAME (NG-nitro-L-arginine methyl ester hydrochloride), an NO synthase inhibitor. Decreased NO catabolism in these mice may have served to counter the effects of NOS inhibition by L-NAME. The current finding that EC-SOD levels that were either higher or lower than controls impaired learning demonstrates that the proper control of brain extracellular O2.- may be more vital than merely reduction of brain extracellular O2.- in maintaining adequate learning function.

Animals↗
PubMed2003

Recovery of spatial memory and persistence of spatial orientation deficits after traumatic brain injury during childhood.

The present study set out to examine the recovery of spatial learning and cognitive mapping skills after severe TBI in childhood. A prospective investigation was carried out with repeated measures. Children with TBI (n = 18) and healthy matched controls (n = 18) were investigated while the children with TBI stayed in a rehabilitation facility (t0) and 4 years later (t1). Children were assessed with the Kiel Locomotor Maze, where they had to remember defined locations in an experimental chamber with completely controlled intra- and extra-maze cues until the learning criterion was reached. During probe trials, cognitive mapping strategies were assessed. Results showed (i) that spatial learning is functionally restituted 4 years post-trauma and (ii) that cognitive mapping skills are still impaired 4 years post-trauma. It was concluded that cognitive performance of children who survived a severe TBI may he overestimated, having far reaching consequences for the children.

Analysis of Variance↗
PubMed2005

[Effects of ibotenic acid lesions to rat's hippocampus CA1 on place and cue learning in Morris water maze].

It is known that the multiple injections of ibotenic acid to the hippocampal CA1 (Cornu Ammonis 1) field of a rat cause cell loss and spatial learning impairment in the place task of Morris water maze. However, no study seems to have been conducted concerning the cue task of the maze. This study examined (1) whether cell loss in the CA1 field produced learning deficits in both the place and cue tasks; (2) whether training could remedy the deficit in spatial learning; and (3) whether the order of place training and cue training could change the performance outcome. Thirty-seven rats of Wistar strain were divided into Place-Cue (PC) group that received place training first and then cue training, and Cue-Place (CP) group that received training in the reverse order. Half rats in each group were damaged in the CA1 field by ibotenic acid injections. Results indicated that damage to CA1 pyramidal cells led to performance deficits only in the place task throughout training, regardless of the sequence of training. The results also indicated that training in the prior task affected learning in the succeeding task, only at the beginning of training, and the effect is transient.

Animals↗
PubMed1988

Investigation into sex-related differences in locomotor activity, place learning and passive avoidance responding in NMRI mice.

Learning abilities of young adult (5-6 weeks) male and female NMRI mice were compared in two tasks involving cognitive functions, namely spatial learning in a water maze and passive avoidance responding. Locomotor activity was also monitored as a putative bias for the results obtained in these learning tests. No sex-related difference was observed either in avoidance responding or in spatial learning using a procedure with the same point of departure throughout testing in the water maze. However, in this test, using a procedure with 3 different points of departure in randomized order day after day, female mice performed better than male mice. The difference was statistically significant on the last acquisition day but was not sustained during a retention trial 72 hr later. Since no sex differences in locomotor activity were observed, the learning effects cannot be attributed to a difference in general activity level.

Animals↗
PubMed1980

Spatial concept learning in preschool children: motoric experiences and verbal repetition as adjuncts to passive listening.

32 preschool children were matched by age, sex, and pretest scores on spatial concept knowledge. Four groups were (a) instruction (see and hear) only, (b) verbal repetition, (c) fine motor treatment (hand manipulation), and (d) gross motor treatment (body movement). The 11 spatial concepts studied were in front of, behind, beside, on top of, under, around, through, right, left, forward, and backward. There was no difference in performance between groups given instruction only and verbal repetition. The motoric groups learned more than the non-motoric groups. Older children knew more concepts initially but did not learn more new concepts than younger children.

Age Factors↗
PubMed1997

Long-term potentiation: a good model for learning and memory?

1. Long-term potentiation (LTP), long-term depression (LTD), and depotentiation of synaptic activity have been suggested to model synaptic plastic changes that occur during learning. Recent reports however show that neither LTP induced by high frequency stimulation (HFS) in the dentate, CA3, or CA1, nor depotentiation in area CA1 of the hippocampus, are reliable models of the learning abilities of rats or mice. LTD cannot reliably be obtained in the hippocampus in vivo and might be an artefact caused by altered inhibitory transmission. 2. Experiments with gene deletion ('knock out') mice strains show that mice that do not express HFS-induced LTP in the dentate are able to learn spatial tasks. 3. Studies of the effect of NMDA receptor blockers also showed that HFS-induced LTP in the dentate is not a model for processes that occur during learning. Studies using drugs that act on metabotropic glutamate receptors showed that HFS-induced LTP or depotentiation of LTP in area CA1 are not models for learning mechanisms either. 4. Neither in vivo recording of naturally-occurring LTP in the dentate nor synaptic saturation experiments in the hippocampus was able to support the theory that LTP occurs during learning. 5. While in vitro experiments are essential tools to investigate cellular and subcellular mechanisms that underlay synaptic transmission, measurements of LTP, LTD, or DP are not reliable models for learning processes and cannot replace experiments with intact animals that learn spatial tasks.

Animals↗
PubMed1999

Learning-induced plasticity of N-methyl-D-aspartate receptors is task and region specific.

Changes in binding of [3H]dizocilpine maleate to N-methyl-D-aspartate-sensitive ion channel receptors were evaluated after learning in order to specify brain regions which might be involved in memory formation. Rats were trained in a five-trial session of 40 min, to discriminate among three odours to obtain food reinforcement. Another group was trained in an eight-arm maze to choose always the same three arms to obtain food reinforcement (nine trials over 150 min). In rats killed 30 min after odour discrimination learning, dizocilpine maleate binding was significantly reduced in hippocampal sub-regions CA3, CA1 and fascia dentata and in frontal cortex. After spatial learning, changes in binding were limited to the amygdala, where a decrease was also observed. These results indicate that functional changes occur in specific brain regions after learning and suggest anatomical loci for further study of synaptic changes at a morphological level, after spatial learning or odour discrimination.

Amygdala↗
PubMed2005

Characterizing learning deficits and hippocampal neuron loss following transient global cerebral ischemia in rats.

The 2-vessel-occlusion + hypotension (2VO + H) model of transient global cerebral ischemia results in neurodegeneration within the CA1 field of the hippocampus, but previous research has failed to demonstrate robust or reliable learning/memory deficits in rats subjected to this treatment. In the present study, sensitive behavioral protocols were developed in an effort to characterize the cognitive impairments following 2VO + H more precisely. Adult rats were exposed to 10 min of bilateral carotid occlusion with simultaneous hypotension. Following recovery, 2VO + H and control rats were subjected to a series of behavioral tests (locomotor activity, sensorimotor battery, water maze [cued, place, learning set], object recognition, and radial arm maze) over an extended recovery period followed by an assessment of neuronal loss in the dorsal hippocampus. The 2VO + H treatment was associated with long-lasting spatial learning deficits in the absence of other behavioral impairments and with neurodegeneration in dorsal hippocampal CA1. Water maze protocols that placed higher memory demands upon the rats (relatively "hard" vs. "easy") were more sensitive for detecting ischemia-induced deficits. We have shown that the use of appropriate behavioral tests (e.g., a relatively difficult place learning task) allowed for the observation of robust spatial learning deficits in a model previously shown to induce relatively subtle behavioral effects. Thus, the 2VO + H model induces both hippocampal neuronal loss and long-term learning deficits in rats, providing a potentially useful model for evaluating therapeutic efficacy.

Animals↗
PubMed1984

Intrahippocampal septal grafts ameliorate learning impairments in aged rats.

Grafts of fetal septal tissue rich in cholinergic neurons were implanted as a dissociated cell suspension into the depth of the hippocampal formation in aged rats with severe impairments in spatial learning abilities. After 2 1/2 to 3 months, the rats with grafts, but not the controls, had improved their performance in a spatial learning test. Their improvement was due, at least in part, to an increased ability to use spatial cues in the task. In all animals the grafts had produced an extensive acetylcholinesterase-positive terminal network in the surrounding host hippocampal formation. Thus, the action of cholinergic neurons in the graft onto elements in the host hippocampal circuitry may be a necessary, but perhaps not sufficient, prerequisite for the observed functional recovery.

Aging↗
PubMed2004

Cognitive and emotional alterations in periadolescent mice exposed to 2 g hypergravity field.

The development of the nervous system is a dynamic process where epigenetic factors play a fundamental role. Both ground-based and space research indicate that exposure to an altered gravitational environment affects rodent neurobehavioral profile and stage of development as well as duration of exposure appear to be critical for the observed effects. The behavioral profile of adolescent (28-day-old) male and female CD-1 mice upon acute 2 g exposure was characterized and emotional/anxiety responses (plus-maze), as well as spatial learning performance (Morris water-maze), were assessed respectively 24 and 48 h after hypergravity exposure. Behavioral observation indicated a transient mild sickness associated with hypergravity, with a decrease in spontaneous activity. Rotation per se induced an increase in emotional/anxious responses and a deterioration of spatial learning acquisition, while hypergravity specifically improved flexibility of spatial orientation.

Animals↗