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Results for “Avoidance Learning”

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PubMed1996

Memory-enhancing effects of benzodiazepines in mice.

In the present study, post-trial effects of clonazepam and diazepam on inhibitory avoidance learning under two different experimental conditions (i.e., 0.25 or 0.75 mA footshock) have been investigated. Both clonazepam (0.5 mg/kg) and diazepam (2 and 8 mg/kg) enhanced retention when administered immediately after the 0.25 mA footshock applied during training of the inhibitory avoidance task. In contrast, clonazepam and diazepam proved ineffective after the 0.75 mA footshock. The results suggest a post-training memory-enhancing effect of clonazepam and diazepam depending on the experimental conditions.

Animals↗

PubMed2004

Neurotoxic lesions of phasic pontine-wave generator cells impair retention of 2-way active avoidance memory.

STUDY OBJECTIVES: The aim of this study was to test the hypothesis that the activation of pontine (P)-wave generator is critical for the posttraining rapid eye movement (REM) sleep-dependent memory processing. DESIGN: Ibotenic acid was microinjected (0.5 microg in 0.05 microL) into the functionally identified P-wave generator in order to destroy the cell bodies and thus to study the effects of their destruction upon waking-sleep states, P-waves, and 2-way active avoidance memory. SETTING: Sleep research laboratory at Boston University School of Medicine. PARTICIPANTS: Adult male Sprague-Dawley rats (N = 27). INTERVENTIONS: Chronically implanted for recording polygraphic signs of sleep and bilateral guide tubes for the local microinjections into the P-wave generator. MEASUREMENTS AND RESULTS: The ibotenic acid produced a small spherical area (< or = 0.35 mm in diameter) of nerve cell loss centered on the P-wave generator. Bilateral lesioning of the P-wave generator decreased P-waves during REM sleep by > 95% without significantly changing the amounts of time spent in wake, slow-wave sleep, or REM sleep. In these P-wave generator-lesioned rats, acquisition of avoidance learning and posttraining wake-sleep changes were identical to those of the sham-lesioned rats. However, in the test trials, after 6 hours of undisturbed sleep-wake, P-wave generator-lesioned rats had no retention of avoidance memory. CONCLUSIONS: These findings, for the first time, provide direct evidence that P-wave-generating cells are critical for normal REM sleep-dependent memory processing. This evidence supports our hypothesis that the P-wave generator in the brainstem may act as an on switch to provide activating input to forebrain structures for sleep-dependent memory processing.

Animals↗

PubMed1993

Cerebral activating properties of indeloxazine HCl and its optical isomers.

The cerebral activating actions of indeloxazine HCl and its optical isomers were evaluated in comparison with those of several selective monoamine uptake inhibitors. The effects of indeloxazine and its optical isomers on monoamine uptake were also determined. Indeloxazine was equipotent to the (-)-isomer in desynchronizing the spontaneous electroencephalogram (EEG) in both mature and aged rats and in accelerating recovery of consciousness induced by concussive head trauma in mice, whereas the (+)-isomer showed about 3 times less potent activity than indeloxazine and the (-)-isomer. The potency of indeloxazine and the (-)-isomer in inhibiting [14C]norepinephrine (14C-NE) uptake was approximately 25-30 times more potent than that of the (+)-isomer. Maprotiline and viloxazine, selective NE uptake inhibitors, also showed facilitatory actions in concussed mice. Selective 5-hydroxytryptamine (5-HT) uptake inhibitors such as citalopram, alaproclate, and zimeldine showed little effect. Indeloxazine, the (-)-, and the (+)-isomers facilitated passive avoidance learning behavior with a bell-shaped response curve in normal rats. The potency of the (+)-isomer in inhibiting [14C]5-HT uptake was equipotent to those of both indeloxazine and the (-)-isomer. While citalopram, alaproclate, and zimeldine also facilitated the acquisition of learning behavior, maprotiline and viloxazine, as well as the dopamine uptake inhibitor amantadine, showed little influence on the latency of step-through behavior. Amitriptyline, with anticholinergic activity, impaired learning behavior. Indeloxazine, its optical isomers, citalopram, alaproclate, and zimeldine also ameliorated cycloheximide-induced disturbance of learning behavior in mice, while maprotiline and viloxazine showed little effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2000

Hypothermia inhibits pentylenetetrazol kindling and prevents kindling-induced deficit in shuttle-box avoidance.

In this study, we evaluated the effects of hypothermic exposure on pentylenetetrazol (PTZ) kindling and the resulting deficit of shuttle-box avoidance learning in rats. Additionally, to acknowledge neuronal cell loss, we estimated the number of toluidine blue-positive cells in different brain regions after PTZ kindling and hypothermia exposure in comparison to different normothermic and hypothermic controls. To obtain hypothermic conditions over a period of up to about 3 h, 30 min after PTZ application the animals were treated with 5 mg/kg chlorpromazine (CP) and 25 min later exposed to 15 degrees C cold water for 5 min. Under these conditions the rectal and the striatal temperature were reduced up to a maximum of 5 degrees C. The additional injection of CP did not influence the development of PTZ kindling. Animals treated with PTZ/CP and exposed to hypothermia did not reach the criterion for kindling. Furthermore, this group of animals did not demonstrate any learning deficit. Forty-eight hours after the last kindling application the number of toluidine blue-stained cells was decreased in the investigated brain regions (hippocampal CA1 and CA3 sector, hilus, and cingular cortex) of kindled rats. Hypothermia protected from cell damage in the hippocampal CA3 sector and in the hilus. Results suggest that the inhibiting effect of hypothermia on the development of kindling and the following learning deficit possibly resulted from the suppression of cell damage in distinct brain structures on PTZ-kindled rats.

Animals↗

PubMed2000

Intrahippocampal spermidine administration improves inhibitory avoidance performance in rats.

Polyamines are polycations present at high concentrations in the mammalian brain. We investigated the effect of an intrahippocampal infusion of spermidine, a polyamine agonist, immediately post-training on the inhibitory avoidance learning paradigm in rats. Bilateral intrahippocampal microinjection of spermidine (0.02-20 nmol) caused an increase in test step-down latencies at low concentrations. Administration of arcaine (0.002-0.2 nmol), an antagonist of the N-methyl-D-aspartate (NMDA) receptor polyamine binding site, did not modify the test step-down latencies. In contrast, co-administration of arcaine and spermidine completely reversed the facilitatory effect of spermidine on the test step-down latencies. These results provide evidence that polyamines may be involved in learning and memory modulation.

Animals↗

PubMed1973

Retrograde amnesia and the "reminder effect": an alternative interpretation.

Recent findings suggest that amnesic agents block the retrieval of stored information. "Reminder" treatments, such as noncontingent punishments given after the production of amnesia for avoidance learning, improve the later retention performance of an animal. The data reported suggest that noncontingent treatments provide an additional learning experience which adds to the retention performance of partially amnesic or poorly trained animals.

Amnesia↗

PubMedDate not supplied

Behavioral and developmental effects of prenatal exposure to pentazocine and tripelennamine combinations.

Long-Evans, hooded rats were intubated with one of four dose combinations of pentazocine and tripelennamine on Days 7-20 of pregnancy: 0:0 (mg/kg pentazocine:tripelennamine), 20:10, 40:0, or 40:20. An additional group had free access to lab chow and water throughout pregnancy. At birth, reduced body weights were evident in all drug-treated offspring. Growth deficits were not noted at 5, 10, 15 or 20 days of age. Three measures of activity were collected at 18 days of age, however, none of these measures were differentially affected as a function of prenatal treatment. At 85 days of age, offspring were tested in a two-way shuttle avoidance paradigm. Although the number of avoidances was not significantly affected by prenatal treatment, offspring exposed to these drugs in combination had shorter response latencies than controls with increased training and made more intertrial crossing responses. Additional offspring were tested for seizure susceptibility at 100 days of age. None of the parameters of seizure activity were significantly affected by prenatal drug treatment. Prenatal exposure to pentazocine and tripelennamine resulted in prenatal growth deficits, increased activity during the intertrial interval and decreased response latencies in a shuttle avoidance learning task, suggesting that this polydrug combination may be associated with some long-term behavioral teratogenic risks.

Animals↗

PubMed1992

Environmental enrichment, neocortical ectopias, and behavior in the autoimmune NZB mouse.

New Zealand Black (NZB) mice have severe autoimmune disease and approximately 40% have cortical ectopias in layer I of sensorimotor cortex. Because the ectopias are similar to those found in dyslexics, NZB mice have been used as an animal model for developmental learning disorders. In addition, these mice have been used as a model of learning deficits associated with autoimmune disease. To determine whether early intervention would affect learning processes in NZB mice, they were reared after weaning in standard cages or enriched environments. They were given a battery of behavioral tests to measure learning, laterality, and activity, after which they were sacrificed and their brains examined for cortical ectopias. The tests sorted into two behavioral sets. Ectopia-associated behaviors included black-white discrimination learning and the Morris spatial maze. As a group, the mice performed well on these tasks. Ectopic mice had poorer performance than non-ectopics on these measures, and environmental enrichment countered the effects of the ectopias. Autoimmune-associated behavior involved two-way avoidance learning in a shuttlebox. Mice were uniformely poor on this task, ectopias did not affect behavior, and environmental enrichment was without benefit. Evidence from this and other studies shows that poor shuttlebox performance is related to the presence of autoimmune disease. Thus, autoimmune disease and cortical ectopias each appear to affect a separate set of behavioral processes. Environmental enrichment is most effective for behavioral impairments mediated via cortical ectopias, but is much less effective, if at all, if autoimmunity is the primary mediator of the impairments.

Animals↗

PubMed1985

Effects of previous REM sleep deprivation on the acquisition of different topographies of discriminated avoidance in the rat.

The effects of REM sleep deprivation (REMSD) for 96 h on discriminated avoidance learning were tested in rats using three different task topographies:in a jumping-box, in a shuttle-box and bar-pressing. The same stimulus relationship and the same methodological controls with regard to the avoidance schedules and to the platform technique were employed. REMSD facilitated the acquisition of the jumping-box response, which was detectable at the end of the third session. REMSD did not interfere in the acquisition of the shuttle-box response since both the experimental and control groups met the criterion by concluding the eighth session without any observable difference in the analyzed parameters. With bar-pressing, neither group reached the learning criterion (80% of avoidance responses throughout two consecutive sessions). We have related these results to the existing hypothesis that REM sleep stimulates the coding of all complex sequences of motor behavior which are necessary for innate behaviors and concluded that the reimbursement of the REM sleep debt after testing facilitated only the acquisition of the jumping-box response through a reprogramming of the motor organization of this innate behavior.

Animals↗

PubMed1990

Effect of pyritinol, a cerebral protector, on learning and memory deficits induced by prenatal undernutrition and environmental impoverishment in young rats.

The study was conducted on 64 CF strain albino rats, which were equally distributed into 8 evenly matched groups following a 2 x 2 x 2 factorial design, by varying three independent factors at two levels: nutrition--normal and undernutrition; environment--enrichment and impoverishment, and drug treatment--vehicle and pyritinol (100 mg/kg, ip). Prenatal undernutrition was induced by restricting the mother's food intake. The environmental enrichment/impoverishment and the vehicle/pyritinol treatments were given during the postweaning period of the pups. The rats were subjected to original and subsequent reversal brightness discrimination learning tests in a single unit T-maze at 8-9 weeks of age. Thereafter, the animals were tested for the passive avoidance learning. The results indicate that undernutrition caused significant original discrimination learning deficits whereas environmental deprivation attenuated both the original and reversal learning performance. Environmental impoverishment attenuated the retention of passive avoidance behaviour but undernutrition had no effect on this paradigm. Pyritinol treatment improved the learning and retention performance of normally reared rats and also attenuated the original and reversal learning deficits induced by parental undernutrition and postweaning environmental impoverishment. The results indicate that pyritinol may be useful in learning and memory deficits induced by malnutrition and environmental deprivation.

Animals↗

PubMed1990

Behavioral effects of pre- and postnatal exposure to a mixture of low chlorinated PCBs in rats.

Polychlorinated biphenyl (PCB)-treated Wistar rats were tested on three different behavioral paradigms. Animals were pre- and postnatally exposed to a technical mixture of PCBs with a chlorine content of 42%. Exposure levels were 0, 5, or 30 mg/kg diet. These conditions did not affect the health of the dams, the litter size or weight, or the physical development of the offspring. Relative liver weights in the offspring, however, were elevated in a dose-dependent manner. Open-field ambulation, active avoidance learning, and operant conditioning on a fixed interval 30-sec schedule (FI-30-sec) were used to evaluate PCB-induced behavioral alterations. Ambulation was increased in 30-mg-treated rats at Day 22, but not at Day 120. There were more avoidance responses and intertrial responses in the 30-mg group than in both other groups. On the FI-30-sec schedule slightly more reactions were emitted by the 30-mg group during the first 10 sec of the interval than by the other animals. More pronounced, however, were the differences between groups in the temporal pattern of responses within the 30-sec interval. It is concluded that in rats PCB exposure causes consistent alterations in all of the tested activity-dependent behaviors.

Animals↗

PubMed1980

Early experience facilitates the development of temperature regulation in the cat.

Thirty kittens were given a 30-min exposure to a moderately cool environment and drop in body temperature was measured. One group was tested every day from age 2 days to 21 days of age. A 2nd group was tested on Days 6-21 and a 3rd group tested only at 19 days of age. The 1st group (tested on Days 2-21) became homeothermic at an earlier age than did the other groups. The data are interpreted to indicate that early exposure to cool temperatures facilitates acquisition of temperature regulation in the cat, and that observed deficits in passive avoidance learning in young cats are not due to increased motor activity produced by a fall in body temperature.

Animals↗

PubMed1993

The effects of brain natriuretic peptide-32 on electroconvulsive shock-induced amenesia in rats. The role of neurotransmitters.

Partial amnesia was induced in rats by electroconvulsive shock (ECS) immediately after passive avoidance learning. This partial amnesia could be prevented by administering porcine brain natriuretic peptide-32 (pBNP-32) into the lateral brain ventricle. The effects of pretreatment with different receptor blockers (haloperidol, atropine, phenoxybenzamine, propranolol, naloxone, bicuculline and methysergide) on the pBNP-32-induced antiamnesia were investigated. In the doses selected, the blockers had no influence on the ECS-induced amnesia. Haloperidol, atropine, phenoxybenzamine and propranolol blocked the antiamnesic action of the peptide, while naloxone, bicuculline and methysergide were ineffective. These results suggest that pBNP-32 may influence learning processes and that the antiamnesic action of this peptide is mediated by dopaminergic, cholinergic alpha- and beta-adrenergic mediator systems.

Amnesia↗

PubMed1994

Effects of physostigmine on male offspring sired by alcohol-treated fathers.

Male rats were intubated with either 3, 2, or 0 g/kg alcohol, twice daily, for 7 months and were then bred to untreated females. At 18 and 58-62 days of age, male offspring were tested for passive avoidance learning. At 82-88 days of age, another group of male offspring were tested for open field activity after receiving 0, 0.1, or 0.4 mg/kg physostigmine, a cholinesterase inhibitor. Offspring sired by alcohol-treated fathers required more trials to reach criterion in the passive avoidance task at 18 days of age, but did not differ significantly at 58-62 days of age. These offspring were more active in the open field compared with controls after receiving vehicle, but did not differ from controls after receiving physostigmine. These results suggest animals sired by alcohol-treated fathers are more active than controls, and this effect is cholinergically mediated. These results are of interest because of their possible relevance to the hyperactivity noted in children born to alcoholic fathers.

Animals↗

PubMed1988

Alterations in the behavior of young and adult rats exposed to aldrin during lactation.

The effects of the administration of aldrin, an organochlorinated pesticide, during the period of lactation were studied on behavior of the litters. The general activity of the young and adult animals was tested in an open-field. In both situations, activity was higher in experimental than in control rats. Experimental animals also showed a higher performance in a hole-board apparatus and in the shuttle-box of two-way active avoidance learning. The results suggest that the insecticide is involved in alterations occurring in the nervous/endocrine systems of the newborn.

Aldrin↗

PubMedDate not supplied

Endogenous BDNF is required for long-term memory formation in the rat parietal cortex.

Information storage in the brain is a temporally graded process involving different memory phases as well as different structures in the mammalian brain. Cortical plasticity seems to be essential to store stable long-term memories, although little information is available at the moment regarding molecular and cellular events supporting memory consolidation in the neocortex. Brain-derived neurotrophic factor (BDNF) modulates both short-term synaptic function and activity-dependent synaptic plasticity in hippocampal and cortical neurons. We have recently demonstrated that endogenous BDNF in the hippocampus is involved in memory formation. Here we examined the role of BDNF in the parietal cortex (PCx) in short-term (STM) and long-term memory (LTM) formation of a one-trial fear-motivated learning task in rats. Bilateral infusions of function-blocking anti-BDNF antibody into the PCx impaired both STM and LTM retention scores and decreased the phosphorylation state of cAMP response element-binding protein (CREB). In contrast, intracortical administration of recombinant human BDNF facilitated LTM and increased CREB activation. Moreover, inhibitory avoidance training is associated with a rapid and transient increase in phospho-CREB/total CREB ratio in the PCx. Thus, our results indicate that endogenous BDNF is required for both STM and LTM formation of inhibitory avoidance learning, possibly involving CREB activation-dependent mechanisms. The present data support the idea that early sensory areas constitute important components of the networks subserving memory formation and that information processing in neocortex plays an important role in memory formation.

Analysis of Variance↗

PubMed2004

Phosphodiesterase type 5 inhibition improves early memory consolidation of object information.

The nitric oxide (NO)-cyclic GMP (cGMP) signaling pathway is assumed to play an important role in processes underlying learning and memory. We used phosphodiesterase type 5 (PDE5) inhibitors to study the role of cGMP in object- and spatial memory. Our results and those reported in other studies indicate that elevated hippocampal cGMP levels are required to improve the memory performance of rodents in object recognition and passive avoidance learning, but not in spatial learning. The timing of treatment modulates the effects on memory and strongly supports a role for cGMP in early stages of memory formation. Alternative explanations for the improved memory performance of PDE5 inhibitors are also discussed. Immunocytochemical studies showed that in vitro slice incubations with PDE5 inhibitors increase NO-stimulated cGMP levels mainly in hippocampal varicose fibers. Reviewing the available data on the localization of the different components of the NO-cGMP signaling pathway, indicates a complex interaction between NO and cGMP, which may be independent of each other. It is discussed that further studies are needed, immunocytochemical and behavioral, to better understand the cGMP-mediated molecular mechanisms underlying memory formation.

3',5'-Cyclic-GMP Phosphodiesterases↗

PubMed1993

Tyr-D-Arg-Phe-beta-Ala-NH2, a novel dermorphin analog, impairs memory consolidation in mice.

Tyr-D-Arg-Phe-beta-Ala-NH2 (TAPA), a novel dermorphin analog with high selectivity and affinity for mu-opioid receptors, was administered intracerebroventricularly to mice before or immediately after training in a one-trial step-down type passive avoidance task. The pre- and post-training administration of TAPA (0.3 and/or 3 ng) impaired retention performance 24 h after training. In particular, the post-training administration of TAPA was much more effective because a lower dose (0.3 ng) of TAPA exclusively inhibited retention performance. The amnesic effects of TAPA were reversed by the mu-selective opioid antagonist beta-funaltrexamine (5 micrograms, i.c.v.). In addition, TAPA (0.3 and 3 ng) had no effects on nociceptive responses in a tail-flick test or on behavioral responses to electric shock during training. These results suggest that activation of mu-opioid receptors impairs passive avoidance learning, resulting in a dysfunction of memory consolidation, without affecting other behavioral responses.

Amino Acid Sequence↗