SEARCH · PubMed Health

Results for “Avoidance Learning”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 883 records · Page 49Linked to original sources

PubMed1994

Acquisition and extinction of jumping, two-way shuttle-box and bar press avoidance responses in malnourished rats: effects of shock intensity.

1. In order to investigate the role of avoidance response and shock intensity in avoidance learning in malnourished rats, three avoidance responses (jumping, two-way shuttle-box and bar press) and three shock intensities (0.4, 0.6 and 1.0 mA) were used. Independent groups of 6 rats were used for each response topography and shock intensity. 2. Malnourished male Wistar rats were suckled by mothers fed a 12% casein diet during the lactation period (0-21 days of age) while the mothers of well-nourished controls received a 25% casein diet. After weaning (21st day), all animals received a commercial lab chow diet until 70 days of age, when the avoidance training started. 3. Malnutrition did not affect the acquisition of the avoidance response, but malnourished groups required more trials to extinguish jumping and two-way shuttle-box. During the acquisition phase all animals learned the jump response faster in comparison to bar press and shuttle-box avoidance responses. Both groups in the acquisition phase responded faster with 1.0 mA when compared to lower intensities (0.6 and 0.4 mA). The malnourished animals showed lower latency of avoidance in the jumping response when compared with well-nourished animals. During the extinction phase there was a significant effect of diet, response topography and shock intensity in the latency to respond and trials to criterion. The increased resistance to extinction in malnourished rats was particularly evident with 1.0 mA in the two-way shuttle-box response. 4. These results suggest that contradictory data related to the acquisition of the avoidance response in malnourished animals cannot be attributed to response topography or variations in shock intensity. Furthermore, our results also indicate that resistance to extinction and latency to respond are appropriate parameters for detecting differences between well-nourished and malnourished animals.

Animals↗

PubMed1977

Preclinical effects: learned behavior.

A review of the previous Marihuana and Health Reports (1971-1975) reveals that an extensive array of experimental procedures and contexts have been used to study the effects of cannabinoids on the performance of learned behavior in animals. These preclinical behavioral experiments have provided a framework for, and guided the design of, subsequent human experimentation. Compared to previous years, only a few experiments pertaining to cannabinoids and learned behavior have appeared during the past two years. By and large these more recent experiments confirm previous findings; no particularly novel procedures have been explored nor have there been dramatically unpredictable results. In part, the decrease in activity in cannabinoid preclinical animal research on learned behavior indicates an increase in human cannabinoid-learning investigations. Several detailed taxonomies of learned behavior are possible. However, for the purposes of the present report, learned behaviors will be categorized into those involving: avoidance learning and aversive control; reinforcement schedules and maze learning; and discrimination learning.

Animals↗

PubMed2005

Memory consolidation induces N-methyl-D-aspartic acid-receptor- and Ca2+/calmodulin-dependent protein kinase II-dependent modifications in alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor properties.

The N-methyl-D-aspartic acid (NMDA) receptor-dependent activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) is necessary for induction of the long-term potentiation of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor-mediated responses in the CA1 region of the hippocampus, a putative model for learning and memory. We analyzed the interplay among NMDA receptor, CaMKII and AMPA receptor during consolidation of the memory for an inhibitory avoidance learning task in the rat. Bilateral intra-CA1 infusion of the NMDA receptor antagonist D-(-)-2-amino-5-phosphonopentanoic acid (AP5) or of the CaMKII inhibitor 2-[N-(2-hydroxyethyl)]-N-(4-methoxybenzenesulfonyl)] amino-N-(4-chlorocinnamyl)-N-methylbenzylamine) (KN-93) immediately after step-down inhibitory avoidance training hindered memory consolidation. Learning of the avoidance response induced the NMDA receptor-dependent translocation of alphaCaMKII to a postsynaptic density-enriched fraction isolated from dorsal CA1 and the autophosphorylation of this kinase at Thr-286. Step-down inhibitory avoidance training increased the quantity of GluR1 and GluR2/3 AMPA receptor subunits and the phosphorylation of GluR1 at Ser-831 but not at Ser-845 in CA1 postsynaptic densities. The intra-CA1 infusion of KN-93 and AP5 blocked the increases in GluR1 and GluR2/3 levels and the phosphorylation of GluR1 brought on by step-down inhibitory avoidance training. Our data suggest that step-down inhibitory avoidance learning promotes the learning-specific and NMDA receptor-dependent activation of CaMKII in the CA1 region of the dorsal hippocampus and that this activation is necessary for phosphorylation and translocation of AMPA receptor to the postsynaptic densities, similarly to what happens during long-term potentiation.

2-Amino-5-phosphonovalerate↗

PubMed1966

Retrograde amnesia: effects of handling and microwave radiation.

Rats that were irradiated with microwaves immediately after the training trial in a one-trial shock-avoidance learning task retained the conditioned avoidance response 24 hours later. However, rats that were handled a few minutes each day for 3 days before the experiment did not retain the response, although they were capable of learning in a later test.

Amnesia↗

PubMed1992

Vitamin B12 improves cognitive disturbance in rodents fed a choline-deficient diet.

The effect of vitamin B12 on learning disturbance was tested in rats. Rats were fed a choline-enriched, choline-deficient, and choline-deficient diet with vitamin B12. Concentrations of acetylcholine in the brain were significantly lower in rats fed a choline-deficient diet than rats fed a choline-enriched diet. Passive avoidance learning shows that rats on a choline-deficient diet showed significantly impaired learning compared to rats on a choline-enriched diet. However, there was no significant difference of acetylcholine in the brain or in the passive avoidance learning between rats fed a choline-enriched and a choline-deficient with vitamin B12 diet. We, therefore, suggest that vitamin B12 potentiates learning in an acetylcholine-deprived brain.

Acetylcholine↗

PubMed1996

Loss of nucleus basalis magnocellularis, but not septal, cholinergic neurons correlates with passive avoidance impairment in rats treated with 192-saporin.

Intraventricular injection of 192-saporin, an immunotoxin directed at the low affinity neurotrophin receptor (p75NGFr), selectively destroys cholinergic neurons in the basal forebrain (CBF). In the present study, we sought to determine if there was a correlation between degree of CBF neuron destruction and degree of passive avoidance behavioral impairment. 192-saporin caused a decrease in the number of p75NGFr + neurons in both nucleus basalis magnocellularis (Nbm) and medial septal nucleus/diagonal band of Broca (MS/DBB). All rats had >95% loss of the p75NGFr + cholinergic neurons in the MS/DBB, but there was variation in the extent of the Nbm cell loss. A significant correlation was found between the severity of impairment of passive avoidance learning and the magnitude of the loss in the number of p75NGFr + neurons in the Nbm. Step-through latency also correlated significantly with the magnitude of loss of AChE histochemical staining intensity in dorsolateral neocortex ipsilateral to the injection of 192-saporin. These data show that >95% loss of cholinergic neurons in MS/DBB is not sufficient to impair passive avoidance learning. However, in the presence of severe loss of cholinergic neurons from the MS/DBB, the resulting deficit in passive avoidance behavior is proportional to the degree of cholinergic neuron loss from the Nbm. These results are interpreted as support for the hypothesis that the cholinergic projection from Nbm to neocortex plays a role in passive avoidance behavior.

Animals↗

PubMed2004

The effects of an essential fatty acid compound and a cholecystokinin-8 antagonist on iron deficiency induced anorexia and learning deficits.

Iron deficiency (ID) is among the most common nutritional diseases, causing deleterious effects that include decreases in cognitive function and weight loss. The ID also induces a reduction in the number and affinity of dopaminergic D2 receptors. The new finding that ID induces an increase in the pancreas cells, leads to the hypothesis that cholecystokinin-8 (CCK-8) is involved in the ID effects. The level of CCK-8 was higher among ID rats, compared with normal rats. The ID rats in our study were anorectic and performed poorly in learning tests (Morris water maze and passive avoidance learning). Essential fatty acids (EFA) mediate dopamine activity and have been found to rehabilitate learning deficits. Treatment with a fatty acid compound blocked both the learning deficits and the anorexia, while a CCK-8 antagonist was successful only against the anorectic effects.

Animal Feed↗

PubMed2005

Neurocognitive and psychotiform behavioral alterations and enhanced hippocampal long-term potentiation in transgenic mice displaying neuropathological features of human alpha-mannosidosis.

Mice with alpha-mannosidase gene inactivation provide an experimental model for alpha-mannosidosis, a lysosomal storage disease with severe neuropsychological and psychopathological complications. Neurohistological alterations in these mice were similar to those in patients and included vacuolations and axonal spheroids in the CNS and peripheral nervous system. Vacuolation was most prominent and evenly distributed in neuronal perikarya of the hippocampal CA2 and CA3 regions, whereas CA1 and dentate gyrus were weakly or not affected. Field potential recordings from CA1 region in hippocampal slices showed enhanced theta burst-induced long-term potentiation (LTP) in alpha-mannosidase-deficient mice. Longitudinal assessment in age-matched alpha-mannosidase-deficient and wild-type littermates, using an extended test battery, demonstrated a neurocognitive and psychotiform profile that may relate to the psychopathological alterations in clinical alpha-mannosidosis. Brainstem auditory-evoked potentials and basic neuromotor abilities were not impaired and did not deteriorate with age. Exploratory and conflict tests revealed consistent decreases in exploratory activity and emotional blunting in the knock-out group. alpha-Mannosidosis mice were also impaired in aversively motivated learning and acquisition of signal-shock associations. Acquisition and reversal learning in the water maze task, passive avoidance learning in the step-through procedure, as well as emotional response conditioning in an operant procedure were all impaired. Acquisition or shaping of an appetitive instrumental conditioning task was unchanged. Appetitive odor discrimination learning was only marginally impaired during shaping, whereas both the discrimination and reversal subtasks were normal. We propose that prominent storage and enhanced LTP in hippocampus have contributed to these specific behavioral alterations in alpha-mannosidase-deficient mice.

Animals↗

PubMed1988

Postnatal application of p-chloroamphetamine or fenfluramine reduces response selection during early ontogenetic development of rat avoidance behaviour.

The influence of one single intraperitoneal application of 50 mumol/kg fenfluramine (FF) or 50 mumol/kg parachloroamphetamine (PCA), respectively, on the 8th postnatal day upon avoidance learning in the early ontogenesis was compared with vehicle-injected controls (NaCl solution). The intoxicated groups were unable to learn a self-shaped avoidance behaviour in a peripheral field avoidance test. They did not find out during the third postnatal week that only central fields of an open field remained unpunished; escape responses along walls were not inhibited in favour of escape into central fields as in controls. The passive avoidance component which is expressed by increasing stay duration in central fields was not developed in FF and PCA rats. The active avoidance component expressed by CS-induced escape before UCS did also not increase in the intoxicated rats. There were no differences of passive avoidance between groups, however, in the fourth week. In the W-maze test after weaning differences between intoxicated groups and controls were evident in the first session and when the schedule was changed. In the reversal learning session the intoxicated groups made more errors. The results support the view that serotoninergic neuron groups participate in the inhibition of incorrect responses and differentiation learning. This early postnatal deficiency may be partly compensated in further development.

Aging↗

PubMed1992

Effects of postnatal ganglioside administration and hypoxia-exposure on the dopamine release from striatal slices, the behaviour and the ganglioside pattern of 2-3 months old rats.

Neonatal rats were injected with a mixture of bovine brain gangliosides (30 mg/kg body weight, s.c.) immediately before the exposure to hypoxia (pO2 = 10 kPa, 10 hrs daily) from the 2nd to the 11th day of life. At the age of 2-3 months the potential protective or restitutive effect of gangliosides on the radiolabelled dopamine release from striatal slices and on the conditioned avoidance learning was studied. No change in the content and the pattern of gangliosides of the rat striata was found after exposure to hypoxia and ganglioside administration, respectively. Both hypoxia exposure and ganglioside treatment of controls increased the dopamine release whereas hypoxic animals treated with gangliosides showed a diminished release. Hypoxia-induced impaired conditioned avoidance learning was improved by ganglioside treatment. The changed release of dopamine and the altered behavioural performance after ganglioside treatment alone indicate the necessity of a very cautious application of gangliosides to the developing brain.

Aging↗

PubMedDate not supplied

Single toluene exposure and changes of response latency in shock avoidance performance.

The behavioral effects of a single exposure to toluene were investigated using shock avoidance performance. Rats were exposed to 2000, 4000, 6000, and 8000 ppm toluene vapor for 4 hr after they acquired shock avoidance learning. Then the effects of toluene on avoidance performance, locomotor activity, and response latencies (RLs) were simultaneously examined for 3 days. Shock avoidance responses were significantly decreased at concentrations of 4000, 6000, and 8000 ppm, but recovered 3-6 hr after the cessation of exposure. The 2000 ppm exposure had no effect on these responses. Locomotor activity was transiently increased at concentrations of 2000 ppm and 4000 ppm, but recovered after 6 hr. Both 6000 ppm and 8000 ppm exposure at first decreased locomotor activity but later increased it. There were biphasic effects, inhibition and excitation, on locomotor activity, and it took 1 day to recover from them. Response latencies were shortened at concentrations of 2000, 6000, and 8000 ppm. That was due to hyperactivity. However, 4000 ppm toluene exposure induced the prolongation of RLs, although ataxia or narcosis were not observed. It was suggested that certain higher nervous functions in the central nervous system (CNS) which controlled timing behavior might be confused.

Animals↗

PubMed2003

High-alcohol-drinking rats exhibit persistent freezing responses to discrete cues following Pavlovian fear conditioning.

We previously reported that high-alcohol-drinking (HAD) rats exhibited selective deficits in active avoidance learning and that those deficits were partially reversed by moderate doses of ethanol under certain training conditions [Pharmacol. Biochem. Behav. 75 (2003) 89]. In that study, we hypothesized that HAD deficits resulted from exaggerated fear in the conditioning context and that the anxiolytic properties of ethanol, along with prior exposure to the conditioning apparatus, were responsible for the facilitated avoidance learning that was observed in HAD rats following moderate doses of ethanol. The current study was designed to test whether HAD rats exhibit behaviors consistent with increased fear in aversive learning contexts. We used a standard Pavlovian fear conditioning paradigm to assess behavioral freezing in HAD (HAD-1 and HAD-2) and low-alcohol-drinking (LAD; LAD-1 and LAD-2) rats. No significant differences were observed between HAD-1 and HAD-2 or between LAD-1 and LAD-2 rats, indicating that the replicate lines performed similarly in this study. Both HAD and LAD rats exhibited robust fear conditioning during training. Although no differences were observed between HAD and LAD rats during fear training, HAD rats failed to extinguish freezing behavior in response to the discrete tone conditional stimulus during subsequent fear retention tests. Thus, HAD rats demonstrated prolonged cue-elicited fear that was resistant to extinction.

Acoustic Stimulation↗

PubMed2005

Molecular correlates of emotional learning using genetically selected rat lines.

The genetic contributions to active avoidance learning in rodents have been well established, yet the molecular basis for genetically selected line differences remains poorly understood. To identify candidate genes influencing this active avoidance paradigm, we utilized the bidirectionally selected Syracuse high- and low-avoidance (SHA and SLA) rat lines that markedly differ in their two-way active avoidance behavior. Rats were phenotyped, rested to allow recovery from testing stress and then hippocampi were dissected for gene expression profiling (Affymetrix U34A chips; approximately 7000 known genes), comparing SLA to SHA. Next, a subset of differentially expressed genes was confirmed by real-time PCR (RT-PCR) in hippocampi. Additional studies at the protein level were performed for some genes. Using triplicate arrays on pooled hippocampal samples, differentially expressed genes were identified by microarray suite 5.0 and robust multi-array average analyses. By RT-PCR analysis in hippocampi, eight genes were nominated as potential candidate genes consistent with the differential expression from the microarray data. Four genes, Veli1 (mlin-7B), SLC3a1, Ptpro and Ykt6p, showed higher expression in SHA hippocampi than SLA. Four genes, SLC6A4, Aldh1a4, Id3a and Cd74, showed higher expression in SLA hippocampi than SHA. The active avoidance behavioral difference between lines probably emerges from 'many small things'. These potential candidate genes generate hypotheses for future testing in human association and rodent studies. Differences in levels of a pleiotropic gene like Ptpro and SLC6A4 suggest that small differences over a lifespan may contribute to large behavioral differences.

Animals↗

PubMed1997

Different effects of postnatal day 1 versus 7 192 immunoglobulin G-saporin lesions on learning, exploratory behaviors, and neurochemistry in juvenile rats.

Passive avoidance learning and retention, as well as locomotor and exploratory behaviors, were assessed in rats after intraventricular 192 immunoglobulin G-saporin injections on either Postnatal Day 1 (PND1) or PND7. PND1-lesioned rats were not significantly impaired on acquisition or retention of passive avoidance. PND7-lesioned rats acquired the task slower than controls, but retention was not affected. PND7-lesioned rats were less exploratory than controls and showed reduced wall rearing. Histological analysis of PND1- and PND7-lesioned rats revealed no neuronal degeneration in hippocampus or cortex. There was a marked reduction of choline acetyltransferase (ChAT) activity in the hippocampus, cortex, and septum in the PND7-lesioned rats and a slight but significant ChAT depletion in the cortex of PND1-lesioned rats. These data suggest that the cholinergic system is critical for the learning of passive avoidance and exploratory behaviors in the developing rat.

Animals↗

PubMed2000

Comparison of methyl anthranilate and denatonium benzoate as aversants for learning in chicks.

Methyl anthranilate (MeA) has been widely used as a taste aversant for domestic chicks in the one-trial passive avoidance learning (PAL) task. However, MeA has a strong smell that may be aversive to chicks. Therefore, odourless denatonium benzoate (DB) has been suggested as an alternative taste aversant in PAL. The present study was designed to compare the efficacy of MeA and DB as aversants in the one-trial PAL task. In this task, young chicks peck a visually conspicuous bead coated with a taste aversant and in a single trial learn to avoid a similar, but uncoated bead at subsequent presentation. In Experiment 1, chicks were trained using a silver-coloured bead coated with 100% MeA, 0.5% DB or distilled water. After 3 h, MeA-trained, but not DB-trained chicks, exhibited significantly higher avoidance of the test bead than water-trained chicks. In Experiment 2, three pre-training presentations of an uncoated red bead preceded training with the silver bead. MeA-trained chicks showed significantly higher avoidance of the test bead than water-trained chicks. The numbers of water- and DB-trained chicks that avoided pecking the test bead were low and not significantly different from each other. However, DB-trained chicks exhibited significantly longer latencies to peck the test bead than water-trained chicks, indicating that they had retained some memory of the task. Thus, 0.5% DB is a weaker aversant than MeA and it does not induce high levels of learning in the one-trial PAL task. However, DB may prove useful for investigating weakly reinforced learning.

Animals↗

PubMed1995

Role of hippocampal nitric oxide in memory retention in rats.

The present study investigated the role of hippocampal nitric oxide (NO) in memory retention of an inhibitory avoidance learning task in rats. The anatomical locus was aimed at the dentate gyrus (DG). Results indicated that intra-DG administration of a NO generator, sodium nitroprusside (SNP), at moderate doses enhanced retention performance in a dose-response fashion in rats. SNP at higher doses, on the other hand, impaired memory retention. Intra-DG injection of a NO inhibitor, L-NG-monomethylarginine (L-MeArg), impaired retention performance at moderate doses. Coadministration of a NO precursor L-arginine (2.9 and 7.2 micrograms) reversed the memory-impairing effect of L-MeArg. An in vitro ADP-ribosylation experiment showed five protein bands with molecular weights around 118, 94, 54, 43, and 39 kDa that were labeled. The labeling intensity of these proteins decreased as the concentration of in vivo SNP increased. These results suggest that hippocampal NO plays a facilitatory role in the memory process of an inhibitory avoidance learning task in rats.

Adenosine Diphosphate Ribose↗

PubMed1989

Memory formation processes in weakly reinforced learning.

Day-old chicks trained on a single-trail passive avoidance learning task, with varying concentrations of the aversive stimulus (methyl anthranilate), truncated retention functions for low concentrations. The retention function for a 20% v/v dilution of methyl anthranilate in absolute ethanol yielded high retention levels until approximately 40 to 45 minutes following learning. This retention function appears to consist of only the short-term and intermediate (phase A) memory stages of Gibbs and Ng's three-stage model of memory formation, with the short-term stage susceptible to inhibition by monosodium glutamate, and the intermediate stage by ouabain and dinitrophenol. The results suggest that processing of memory into the relatively permanent long-term stage may depend on the strength of the reinforcer in aversive learning.

2,4-Dinitrophenol↗

PubMed1989

Antagonism of NMDA receptors impairs acquisition but not retention of olfactory memory.

Prompted by evidence pointing to a key role of the N-methyl-D-aspartate (NMDA) receptor system in the induction of long-term potentiation and possibly in the formation of some types of memory, we examined the effect of chronic intraventricular administration of D-amino-phosphono-valeric acid (AP5), a competitive NMDA receptor antagonist, on olfactory discrimination and avoidance learning. These two tasks were selected because they are affected to very different degrees by damage to the hippocampus and other telencephalic structures rich in NMDA receptors. Twenty rats previously trained to solve a series of discriminations between two simultaneously presented odors were infused with either 20 mM D-AP5 or saline (n = 10 per group) for 14 days. An important and unusual feature of the paradigm was that it permitted a comparison of drug effects on acquisition of new discriminations versus retention of old ones. Animals treated with AP5 made significantly more errors than did saline controls in acquiring discriminations between low-intensity odors presented with long intertrial intervals (ITIs). However, no deficit was observed when short ITIs (less than 2 min) or strong odors were used. Animals treated with AP5 had no difficulty in recognizing odors on which they were trained before administration of the drug. After exhaustion of the pumps, performance of the AP5 group was indistinguishable from that of the control group. One-way active avoidance learning was not affected by chronic infusion of AP5. Several possibilities are discussed that could account for the selective olfactory learning deficit.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗