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PubMed1995

Maze learning in aged rats is enhanced by phenserine, a novel anticholinesterase.

A new generation of cholinesterase inhibitors is expected to overcome some limitations of the therapeutic use of anticholinesterases. Phenserine is a long-acting and selective inhibitor of acetylcholinesterase with a preferential brain uptake. We have assessed the effects of chronic phenserine tartrate treatment on performance of aged Fischer-344 rats in the 14-unit T-maze. Phenserine (1-3 mg kg-1, i.p.) treatment for 5 days significantly reduced the number of errors made in the Stone maze. Other performance variables were also improved. No side effects were noted across 5 days treatment at doses of 1-2 mg kg-1. Phenserine can therefore improve the performance of aged rats in this complex maze task without producing obvious side effects.

Aging↗

PubMed1979

Effect of scopolamine on maze learning performance in humans.

Scopolamine was administered orally to volunteers who were required to learn a digit memory task and a tactile maze task. Comparison of their performance with that under control drugs suggests that blockage of central cholinergic synapses may have a larger effect on spatial memory than on nonspatial memory. Subjects tended to make more errors under scopolamine and to insert extra turns in drawings of the maze.

Humans↗

PubMed1998

Changing patterns of brain activation during maze learning.

Recent research has found that patterns of brain activation involving the frontal cortex during novel task performance change dramatically following practice and repeat performance. Evidence for differential left vs. right frontal lobe activation, respectively, during episodic memory encoding and retrieval has also been reported. To examine these potentially related issues regional cerebral blood flow (rCBF) was measured in 15 normal volunteers using positron emission tomography (PET) during the naive and practiced performance of a maze task paradigm. SPM analysis indicated a largely right-sided, frontal lobe activation during naive performance. Following training and practice, performance of the same maze task elicited a more posterior pattern of rCBF activation involving posterior cingulate and precuneus. The change in the pattern of rCBF activation between novel and practiced task conditions agrees with results found in previous studies using repeat task methodology, and indicates that the neural circuitry required for encoding novel task information differs from that required when the same task has become familiar and information is being recalled. The right-sided preponderance of activation during naive performance may relate to task novelty and the spatially-based nature of the stimuli, whereas posterior areas activated during repeat performance are those previously found to be associated with visuospatial memory recall. Activation of these areas, however, does not agree with previously reported findings of left-sided activation during verbal episodic memory encoding and right-sided activation during retrieval, suggesting different neural substrates for verbal and visuospatial processing within memory.

Adult↗

PubMed2001

Effects of neocortical ectopias and environmental enrichment on Hebb-Williams maze learning in BXSB mice.

Approximately 40-60% of BXSB mice have neocortical ectopias, a developmental anomaly characterized by migration of neurons into the neuron-sparse layer I of cortex. Previous studies have shown that ectopic BXSB mice have superior reference, but inferior working, memory on spatial tasks. Female BXSB mice were housed either in an enriched environment or in standard cages at weaning. Subsequently, these animals were tested on four of the Hebb-Williams mazes in a water-based version of this maze. Theoretically, two of the maze configurations placed greater emphasis on reference memory to find the goal, whereas the other two favored working memory. Ectopics reared in standard housing conditions were better than nonectopics on mazes that favored the use of reference memory, but poorer on mazes that favored working memory. In contrast, subjects raised in the enriched environment showed no ectopia differences. A comparison of enriched and standard housing conditions found that the enriched animals had better reference memory but poorer working memory. The latter effect may be because the enriched environment, although more stimulating, did not change in time or space; and other researchers have shown that daily replacement of stimuli in complex environments is correlated with better working memory.

Animals↗

PubMed1999

Geophysical variables and behavior: LXXXVII. Effects of synthetic and natural geomagnetic patterns on maze learning.

12 normal male albino rats were exposed or not exposed in their home cages for 5 min. and 50 sec. once every hour 8 times per night to a 7-Hz square-wave magnetic field whose amplitudes were shifted by about 50 nT approximately every 10 sec. Although there were no statistically significant differences between the two groups for numbers of working errors, numbers of reference errors, or speed during the acquisition of an Olton (8-arm) maze, the strength of the group differences (F ratios) for daily working errors was reduced (rho = .70) if there had been enhanced geomagnetic activity during the time of the night when the experimental fields were present.

Animals↗

PubMed2005

Phosphodiesterase inhibition by sildenafil citrate attenuates a maze learning impairment in rats induced by nitric oxide synthase inhibition.

RATIONALE: The nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) signal transduction pathway has been implicated in some forms of learning and memory. Recent findings suggest that inhibition of phosphodiesterase (PDE) enzymes that degrade cGMP may have memory-enhancing effects. OBJECTIVES: We examined whether treatment with sildenafil citrate, a PDE type 5 inhibitor, would attenuate a learning impairment induced by inhibition of NO synthase [60 mg/kg N(omega)-nitro-L-arginine methyl ester (L-NAME), i.p.]. METHODS: Rats were pretrained in a one-way active avoidance of foot shock in a straight runway and, on the next day, received 15 training trials in a 14-unit T-maze, a task that has been shown to be sensitive to aging and impairment of central NO signaling systems. Combined treatments of L-NAME or saline and sildenafil (1.0, 1.5, 3.0, or 4.5 mg/kg, i.p.) or vehicle were given 30 and 15 min before training, respectively. Behavioral measures of performance included entries into incorrect maze sections (errors), run time from start to goal (latency), shock frequency, and shock duration. RESULTS: Statistical analysis revealed that L-NAME impaired maze performance and that sildenafil (1.5 mg/kg) significantly attenuated this impairment. Control experiments revealed that administration of L-NAME alone did not significantly increase latencies in a one-way active avoidance test and that different doses of sildenafil alone did not significantly alter complex maze performance. CONCLUSIONS: The results indicate that sildenafil may improve learning by modulating NO-cGMP signal transduction, a pathway implicated in age-related cognitive decline and neurodegenerative disease.

Animals↗

PubMed2006

Post-training intra-striatal scopolamine or flupenthixol impairs radial maze learning in rats.

Systemic treatments with acetylcholine (ACh) or dopamine (DA) receptor antagonists during hours 0-4 but not during hours 5-8 following training on a radial arm maze (RAM) or lesions of the dorsal striata impair learning. This suggested that intra-striatal infusions of ACh or DA receptor antagonists during hours 0-4 following training may impair learning. Rats were randomly assigned to groups (ns=5-11) receiving dorsal striatal infusions of the ACh receptor antagonist scopolamine (0-18 microg/microL at 0 and 2h or at 4 and 6h after training), the DA receptor antagonist cis-flupenthixol (0-25 microg/microL at 0, 4 or 12h after training) or the inactive isomer trans-flupenthixol (6 microg/microL at 0 h after training). Scopolamine and cis-flupenthixol impaired the habit-learning version of the task. Given after hours 0-4 following training, the effects of scopolamine were diminished but those of cis-flupenthixol were not. Trans-flupenthixol produced less impairment than cis-flupenthixol. Results suggest that ACh and DA receptors in the dorsal striatum during hours 0-4 following training play a role in habit learning.

Acetylcholine↗

PubMed1997

Reciprocal changes in expression of mRNA for nerve growth factor and its receptors TrkA and LNGFR in brain of aged rats in relation to maze learning deficits.

Quantitative in situ hybridization was used to examine the expression of mRNA for nerve growth factor (NGF) and its receptors, p140Trk (TrkA) and p75LNGFR (LNGFR), in different brain regions of adult (3-month-old) and aged (27-month-old) Wistar rats. The brain regions studied were hippocampus (dentate gyrus, CA3 region), basal forebrain (medial septum, diagonal band) and caudate-putamen. Prior to hybridization histochemistry behaviorally impaired as well as severely impaired animals were selected from a large group of old rats according to their performance in the Morris water maze. The impaired rats showed longer escape latencies and, thus, implicitly impaired performance in the place version of the task, but did not differ from adult controls on the platform crossing measure registered during the spatial probe trial. The severely impaired rats were significantly impaired on both measures, both in comparison with the adult animals and in comparison with the impaired aged rats. Inspection of the hippocampus revealed no age- or performance-related changes in NGF mRNA levels. The overall expression of TrkA mRNA in basal forebrain and caudate was found to be decreased in the impaired (-20%) as well as the severely impaired aged rats (-17%). A significant increase in p75LNGFR mRNA was found in the basal forebrain of the impaired rats in comparison with the severely impaired aged rats (+35%) and adult animals (+33%). These findings show that age-related maze performance deficits are accompanied by a decrease in basal forebrain and striatal TrkA mRNA expression. The increase in basal forebrain LNGFR mRNA levels observed in impaired, but not severely impaired, aged rats may reflect an early manifestation of processes underlying age-related cognitive deficits and may constitute a restorative and/or compensatory mechanism, since these rats displayed fewer deficits in navigation of the maze.

Aging↗

PubMed1993

Enhancement of Y-maze learning by piracetam, 2-thio-1-pyrrolidine-acetamide and 2-thio-1-pyrrolidine-thio-acetamide in rats.

Learning of rats given either piracetam, 2-thio-1-pyrrolidine-acetamide (thioacet) or 2-thio-1-pyrrolidine-thio-acetamide (thiothio) was studied in order to investigate nootropic effects of the compounds. Learning ability was measured using a Y-maze with water reward for the correct choice in a black-white discrimination task. Thioacet and thiothio enhanced learning ability of the rats at doses that were 2.5-10 times lower than those required for obtaining nootropic effects of piracetam. Thus the thio-derivatives of piracetam might be of value for studying mechanisms of action of nootropic drugs.

Animals↗

PubMedDate not supplied

Prenatal exposure to sodium phenytoin in rats induces complex maze learning deficits comparable to those induced by exposure to phenytoin acid at half the dose.

Gravid Sprague-Dawley CD (VAF) rats were administered sodium phenytoin suspended in corn oil by gavage once per day on embryonic days 7-18 at a dose of 100 mg/kg. Controls were administered corn oil alone by gavage on E7-18. Litters were randomly culled to 10. Offspring were regularly weighted, mortality noted, and males checked for preputial separation. At approximately 50 days of age offspring were evaluated in a straight water-filled channel for swimming proficiency and motivation to escape. Following this, rats were tested in the Cincinnati multiple T-water maze and scored for errors, latency to find the goal, and presence of phenytoin-induced abnormal circling behavior while swimming. Sodium phenytoin-exposed dams gained weight normally and delivered normally. Offspring mortality in the sodium phenytoin group was not increased above controls. No treatment effects on preputial separation or offspring growth were observed. No differences between groups in swimming proficiency in straight channel performance were obtained. In the Cincinnati maze, phenytoin offspring committed significantly more errors and had longer latencies to find the goal than controls. Among the phenytoin offspring, those exhibiting abnormal circling committed more errors than noncircling animals. When compared to previous data using the same maze and test protocol, it was found that 100 mg/kg of sodium phenytoin induced performance deficits similar to those induced by a dose of 200 mg/kg of phenytoin acid. Accordingly, the present data help explain why other investigators have reported sodium phenytoin to be more developmentally neurotoxic than phenytoin acid. Because the prenatal neurotoxic effects seen with the salt of phenytoin occur at lower doses, it suggests that phenytoin is more developmentally neurotoxic than previously believed.

Animals↗

PubMed2006

Long-term effects of neonatal basal forebrain cholinergic lesions on radial maze learning and impulsivity in rats.

We examined long-term behavioural effects of neonatal lesions of the cholinergic basal forebrain obtained by intracerebroventricular injections of 192 IgG saporin (192 IgG-Sap). Five-month-old Wistar male rats (injected with 192 IgG-Sap or phosphate-buffered saline on postnatal day 7) were tested using operant chambers with two nose-poking holes, delivering one food pellet immediately or five pellets after a delay. The length of delay progressively increased over days (from 0 to 100 s). When compared with controls, 192 IgG-Sap rats showed a slight preference for smaller immediate over larger delayed rewards, thus indicating elevated intolerance to delay (i.e. more impulsivity). Sibling animals were tested in a computerized radial maze (baited vs. nonbaited arm procedure). 192 IgG-Sap rats appeared slower than controls in accomplishing the task. The neonatal 192 IgG-Sap lesion did not alter cortical levels of serotonin and/or its metabolites, but induced a marked cortical cholinergic loss. Our data suggest that a prolonged basal forebrain cholinergic hypofunction produces (i) an impairment in cognitive performances that is detectable only when highly complex tasks are used; (ii) a slight enhancement of the impulsive behavioural profile. This animal model may thus be useful to investigate some cognitive deficits and other secondary symptoms seen in Alzheimer's disease.

Alzheimer Disease↗

PubMed2001

Impairment of maze learning in rats by restricting environmental space.

We previously reported that the restriction of environmental space attenuates spontaneous locomotor activity and hippocampal acetylcholine release. To examine the effect of the restriction of environmental space on spatial learning function, male rats were individually housed in a cylindrical large cage (diameter=35 cm) or small cage (diameter=19 cm) for 5 days. Eight-arm radial maze performance was examined to evaluate spatial learning and memory functions. The task was performed once a day between 21:00 and 22:00 h in the dark phase. Although all rats learned and performed the task, those in the small cage had lower scores and took more trial time than those in the large cage. These results suggest that the restriction of environmental space impairs spatial learning in the dark phase in rats.

Acetylcholine↗

PubMed1995

Holeboard maze-learning deficits and brain monoaminergic neurotransmitter concentrations in rats after intracerebroventricular injection of 3-bromopyruvate.

3-Bromopyruvate is a suicide inhibitor of pyruvate dehydrogenase complex in brain homogenates, and after intracerebral injection reduces acetylcholine tissue content and muscarinic cholinergic receptors in brain cortex and hippocampus for extended periods of time. A stereotaxic injection of 0.2 mumol 3-bromopyruvate was given twice into the cerebral ventricles of male Wistar rats. Ten weeks later, the animals were tested for learning deficits in a food-motivated complex holeboard test. 3-Bromopyruvate-treated rats showed an increased number of visits to nonfood-baited holes over a 5-day testing period (four trials per day) compared to sham-operated control rats, an increased number of visits to food-baited holes over the first 2 days of the testing period and an increased time for completing the task. There were no changes in brain monoaminergic neurotransmitter concentrations compared to controls. The results indicate that long-term learning deficits in a spatial discrimination paradigm are caused by 3-bromopyruvate, which might be related to a cholinergic deficit induced by a primary inhibition of brain glucose metabolism at the step of pyruvate dehydrogenase complex. This animal model may be useful for behavioral studies in relation to neurodegenerative diseases like dementia of Alzheimer type.

Animals↗

PubMed2001

Effect of innate direction bias on T-maze learning in rats: implications for research.

Adult, male Wistar rats showed substantial left (22.2%) or right (52.8%) bias in spontaneous arm preference in the T-maze; this bias was consistent over 2 days of testing separated by a 30 day interval. Left and right biased rats learnt very rapidly when trained to enter the arm ipsilateral to the bias; learning was significantly poorer or did not occur in the contralateral arm. This contralateral learning difficulty was particularly evident when transfer of learning was assessed. Right-biased rats were more impaired in contralateral learning than left-biased rats. Unbiased rats (25%) also showed learning difficulties. This study has important implications for spatial tasks of learning and memory; with specific reference to the T maze, it is concluded that animals should be preselected for capacity to learn in both arms, randomization into experimental and control groups should be stratified for spontaneous arm bias, and original learning should be directed towards the contralateral arm while transfer of learning, if required, can be directed into the ipsilateral arm.

Animals↗

PubMed1998

Neuroprotective concentrations of the N-methyl-D-aspartate open-channel blocker memantine are effective without cytoplasmic vacuolation following post-ischemic administration and do not block maze learning or long-term potentiation.

The potential of most N-methyl-D-aspartate antagonists as neuroprotectants is limited by side effects. We previously reported that memantine is an open-channel N-methyl-D-aspartate blocker with a faster off-rate than many uncompetitive N-methyl-D-aspartate antagonists such as dizocilpine maleate. This parameter correlated with memantine's known clinical tolerability in humans with Parkinson's disease. Memantine is the only N-methyl-D-aspartate antagonist that has been used clinically for excitotoxic disorders at neuroprotective doses. Therefore, we wanted to investigate further the basis of its clinical efficacy, safety, and tolerability. Here we show for the first time for any clinically-tolerated N-methyl-D-aspartate antagonist that memantine significantly reduces infarct size when administered up to 2 h after induction of hypoxia/ischemia in immature and adult rats. We found that at neuroprotective concentrations memantine results in few adverse side effects. Compared to dizocilpine maleate, memantine displayed virtually no effects on Morris water maze performance or on neuronal vacuolation. At concentrations similar to those in brain following clinical administration, memantine (6-10 microM) did not attenuate long-term potentiation in hippocampal slices and substantially spared the N-methyl-D-aspartate component of excitatory postsynaptic currents, while dizocilpine maleate (6-10 microM) or D-2-amino-5-phosphovalerate (50 microM) completely blocked these phenomena. We suggest that the favorable kinetics of memantine interaction with N-methyl-D-aspartate channels may be partly responsible for its high index of therapeutic safety, and make memantine a candidate drug for use in many N-methyl-D-aspartate receptor-mediated human CNS disorders.

Animals↗

PubMed1995

Radial maze learning using exclusively distant visual cues reveals learners and nonlearners among inbred mouse strains.

Spatial working memory on the radial maze was studied in 8 groups of isogenic mice. The device and procedure were specially designed to prevent the mice from using a response strategy or taking advantage of olfactory trails or other proximal cues. The results showed that the strains of mice were clearly split between those which succeeded (C57BL/6, DBA/2, CB6F1, B6D2F1) and those which failed (NZB, CBA, C3H/HE, BALB/c) to learn the task. A second experiment established that when more extended training was given, the four strains which had performed poorly in experiment 1 still did not improve their performance. In the conclusion, we discuss the possible reasons for the deficits of nonlearners and emphasize the importance of using proper tools to ensure the unambiguous assessment of the cognitive processes underlying behavioral adaptation.

Animals↗

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↗

PubMed2002

Chronic treatment with the antidepressant amitriptyline prevents impairments in water maze learning in aging rats.

Increasing evidence links chronically elevated glucocorticoid levels and cognitive impairments in a subpopulation of aged rodents and humans. Antidepressant drugs improve hypothalamic-pituitary-adrenal axis feedback regulation and reduce plasma glucocorticoid levels. Decreasing the cumulative lifetime exposure to glucocorticoid excess by long-term exposure to antidepressants may prevent the emergence of cognitive impairments in aged rats. To test this hypothesis, we treated middle-aged male Lister hooded rats (16 months) with amitriptyline until they were 24 months of age, and their cognitive function was assessed in the water maze. Performance in the spatial learning task declined significantly with aging (p < 0.01), with 33% of aged controls showing poorer (<2.5 SD) probe test performance than young controls. Amitriptyline treatment from midlife preserved water maze performance with aging (p < 0.01 compared with aged controls) and significantly (p < 0.01) reduced the proportion of poor performers (7%). Measures of anxiety-related behaviors in the elevated plus-maze were significantly (p < 0.05) decreased in the aged rats after amitriptyline. Furthermore, evening plasma corticosterone levels were reduced (30% decrease; p < 0.01 compared with aged controls) after 6 months of amitriptyline. These data suggest that long-term treatment with amitriptyline decreases the prevalence of cognitive impairment in aged rats and that this may, in part, be a consequence of reduced plasma corticosterone levels and reduced anxiety.

Administration, Oral↗