PubMed Health⌕ Search

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 73 records · Page 4Linked to original sources
PubMed1979

Effects of fetal and early postnatal thiamin deficiency on avoidance learning in rats.

Thiamin deficiency was induced in two groups of young rats during two stages of growth: deficiency 1, from 8 days prepartum to 10 days postpartum or deficiency 2, from 1 to 18 days postpartum. The deficiency was reversed by thiamin injections for 5 days and return to a normal diet following which animals were tested at 35 days of age. Body weights at 21 and 36 days of age were not significantly reduced by the deficiency nor was brain weight affected. Activity levels were not significantly reduced by deficiency 1 but were reduced in deficiency 2. Both active and passive avoidance learning were significantly impaired in both deficiency 1 and 2, a finding which could not be attributed to alterations in pain sensitivity, motor ability or reduced activity levels. The results indicate that the developing brain is vulnerable to reduced thiamin intake and that the period of vulnerability may be different for activity and avoidance learning.

Aging↗
PubMedDate not supplied

Repeated toluene exposure and changes of response latency in shock avoidance learning.

Behavioral effects of repeated exposure to toluene were investigated. After 1, 3, and 6 weeks exposure to toluene at 1000 and 2000 ppm, all rats received shock avoidance training. Toluene-exposed rats could acquire shock avoidance learning and there was no significant difference between exposed rats and control rats. Analyzing response latencies (RLs) of avoidance responses, control rats shifted them to a longer RL and at last they learned to perform avoidance responses with specific RLs (3-4 sec). However, rats exposed to 1000 ppm toluene for 1 week and to 2000 ppm toluene for 1 week and 3 weeks, did not learn to respond with specific RLs. Rats exposed to 1000 ppm and 2000 ppm toluene for 6 weeks did not shift to longer RLs. It was suggested that repeated exposure to toluene vapor ranging up to 2000 ppm had no influence on the acquisition of shock avoidance learning, but caused some functional impairments of higher nervous functions.

Animals↗
PubMed1986

The effects of cholinergic drugs support an avoidance learning hypothesis of brief footshock-induced analgesia.

Rats were tested for tail-flick responses and then immediately subjected to footshock for 30 sec. This procedure induced analgesia, i.e. prolonged the latency of the tail-flick response, which was maximal immediately after the shock and decayed to normal levels within 2 hr. No analgesia occurred if either the analgesia test before the shock or the shock itself was omitted. The dependence of the analgesia on the association between the test before the shock plus the shock, suggests that this was a form of avoidance learning. The effects of drugs injected immediately after the shock were determined on latency of the tail-flick response, measured 2 hr later. Drugs known to improve memory, including physostigmine, pramiracetam and the muscarinic agonists, oxotremorine and RS 86, selectively induced analgesia in rats subjected to test before the shock plus the shock, thereby supporting a hypothesis of avoidance learning. Neostigmine and atropine methyl nitrate had no effect, indicating that the effects were mediated centrally. The learning effects were distinguishable from analgesia induced by drugs, since morphine increased analgesia regardless of the presence or absence of the test before shock or the shock. Also, naloxone, which had no effect per se, blocked analgesia induced by morphine but enhanced physostigmine-induced analgesia. Neither chlordiazepoxide nor D-amphetamine produced any changes in the latency of the tail-flick responses indicating that neither anxiolytic/muscle relaxant nor stimulant actions were involved.

Analgesia↗
PubMed1990

Effects of NMDA receptor antagonists on passive avoidance learning and retrieval in rats and mice.

The effects of NMDA antagonists on passive avoidance learning, shock sensitivity and locomotor activity were examined. Pre-training administration of the antagonists 3-((+-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) and (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801) in mice and rats resulted in impaired performance in a retention test 24 h later. No such impairment resulted from immediate post-training administration of either compound in either species. In addition neither compound, given only before the retention test, reduced the retention latencies of mice. In rats CPP was similarly ineffective whereas MK-801 reduced retention latencies, but only at a dose which significantly elevated locomotor activity at the time of the retention test. As assessed by vocalization threshold in mice and by the proportion of animals vocalizing in response to the passive avoidance training shock, neither compound produced analgesia. The vocalization threshold was, in fact, slightly reduced by both compounds. MK-801, but not CPP, stimulated locomotor activity in mice. These results indicate that in the passive avoidance task activation of NMDA receptors is involved in memory formation, but is not critical for the maintenance of memory or its retrieval.

Animals↗
PubMed1991

Genetic determinants of individual differences in avoidance learning: behavioral and endocrine characteristics.

Bidirectional genetic selection for good and poor active avoidance learning in a shuttle box has been carried out in three independent laboratories using remarkably similar discrete-trial training procedures. The resulting strains are known as the Roman High and Low Avoidance (RHA and RLA), the Syracuse High and Low Avoidance (SHA and SLA) and the Australian High and Low Avoidance (AHA and ALA) strains, respectively. An additional unidirectionally selected strain, known as the Tokai High Avoider (THA) strain was developed in Japan using a free-operant Sidman avoidance procedure in a Skinner box. This paper reviews the selection of the Syracuse strains, enumerates the various behavioral and endocrine characteristics of the strains, and compares them to the other similarly selected strains. The behavioral work suggests that genetic selection from diverse breeding stocks has resulted in common characteristics that differentiate the strains in the emotional, not learning, domain. The endocrine data, however, are somewhat at odds. The Syracuse strains differentiate one way with respect to endocrine function, and the Roman strains differentiate in the opposite way. We suggest, therefore, that the endocrine correlates are not tightly linked to the avoidance genotype. Genetic analysis of all of the selected strains for both the avoidance phenotype and the endocrine correlates will be needed to test this hypothesis.

Animals↗
PubMed1992

Effect of diazepam on successive negative contrast in one-way avoidance learning.

The effect of administration of diazepam on successive negative contrast in one-way avoidance learning was examined in rats. Contrast was induced by shifting rats from a large reward, 30 s spent in the safe compartment, to a small reward, 1 s spent in the safe compartment. IP administration of 2 mg/kg diazepam eliminated this negative contrast. Moreover, this effect is dose dependent, with doses of 2 and 2.5 mg/kg, but not 0.5 mg/kg, effective in reliably reducing contrast. These results suggest the existence of similar or common underlying mechanisms in both aversive and appetitive contrast effects; they are discussed in light of the current theories of frustrative nonreward and as a mean of studying the behavioral and biological mechanisms of anxiety.

Animals↗
PubMed1976

Stimulation of rat medial or sulcal prefrontal cortex during passive avoidance learning selectively influences retention performance.

Low-level unilateral electrical stimulation was delivered during passive avoidance learning through a bipolar electrode to the prefrontal cortex of the adult albino rat. No brain stimulation was applied during a retention test measured 24 h later. Ventromedial prefrontal cortex stimulation produced retention impairment over and above that observed with chronic electrode implantation. Sulcal cortex stimulation, in contrast, actually attenuated the retention deficit produced by chronic implantation in the sulcal cortex. Stimulation of an afferent common to both prefrontal regions, the dorsomedial thalamus, resulted in retention disruption, but stimulation of another common afferent, the locus coeruleus, did not. Acquisition of the inhibitory response was not affected by stimulation of any of the above brain regions. The present results demonstrate, again, that the functional role in memory of particular brain regions can be dissected by low-level electrical stimulation. The functional separation of rat sulcal and medial cortices revealed by the effects of stimulation suggests that these prefrontal subfields subserve different functions in the information storage process.

Animals↗
PubMed1990

Avoidance learning under hypo and hyperglycemia in rats.

Learning behaviour under different glycaemic conditions were studied in albino rats using an avoidance box. When insulin and glucose levels were low after fasting, animals showed delay in avoidance learning. But there was no change in acquisition of learning after hypoglacaemia induced by insulin. This difference in behaviour under hypoglycaemia of almost similar severity is possibly due to difference in its rate of induction and activation of counter regulatory neuro-endocrine mechanisms. Diabetic (alloxan) rats failed to improve learning. Besides, hyperglycemia, other factors like metabolic disturbances, cytotoxic effects of alloxan may have inhibited learning in this group. Hypo or hyperglycemia disturb the function of neuronal substrates responsible for learning and memory.

Animals↗
PubMed1992

Active avoidance learning in old rats chronically treated with levocarnitine acetyl.

The aging laboratory animal is recognized as a suitable experimental model for the investigation on drugs potentially able to retard the age-dependent decline in cognitive functions. There is robust evidence that levocarnitine acetyl (ALCAR), the acetyl derivative of carnitine, when administered chronically, prevents some age-related deficits of the central nervous system, mainly at the hippocampal level. On the basis of this evidence and because learning of active avoidance was demonstrated to become impaired with age, we decided to investigate the effect of ALCAR in rats. For statistical evaluation of results, the Cluster Analysis technique was chosen. This procedure pointed out the great heterogeneity of the old population and allowed the classification of the animals into homogeneous groups according to their response pattern. The effect of ALCAR was evident in the higher number of treated old animals yielding escape responses, indicating that ALCAR can preserve, at least partially, learning and memory from the natural decay occurring with age.

Acetylcarnitine↗
PubMed1975

Dose-response effects of d-amphetamine on passive avoidance learning in the rat.

Trials and errors to learning a passive avoidance response were assessed in 63 albino rats injected subcutaneously with d-amphetamine, in amounts ranging from 0-7 mg/kg body weight. Both measures indicated dose-response effects on responding; animals under either low or high doses of d-amphetamine made significantly less errors and took significantly fewer trials to learn the response than did middle dosage animals. The scores of the lower and higher dosage animals did not differ from the nondrug control group. Results are discussed in terms of amphetamine stereotypy.

Animals↗
PubMed1990

[The development of theories of avoidance learning and its application to behavioral pharmacology].

How the development of theories changed the definition of avoidance behavior was discussed. Three major theories of avoidance learning; the two-process theory, the species-specific defense reactions hypothesis, and the cognitive expectancy theory were reviewed. Very few innovations were brought to the experimental apparatuses and procedures by which these theories were tested. The paradigms have been applied without any theoretical considerations. Therefore, I claim here that the modification or renewal of experimental paradigms will be needed to make suitable animal models for psychopharmacology.

Animals↗
PubMed1991

Effects of cingulate cortical lesions on avoidance learning and training-induced unit activity in rabbits.

This study extends an ongoing analysis of the neural mediation of discriminative avoidance learning in rabbits. Electrolytic lesions encompassing anterior and posterior cingulate cortex (area 24 and 29) or ibotenic acid lesions in area 24 only were made prior to avoidance conditioning wherein rabbits learned to step in response to a tone conditional stimulus (CS+) in order to avoid a brief, response-terminated 1.5 mA. foot-shock unconditional stimulus (US). The US was presented 5 s after CS+ onset, in the absence of a prior stepping response. The rabbits also learned to ignore a different tone (CS-) not followed by the US. Multi-unit activity of the caudate and medial dorsal (MD) thalamic nuclei, projection targets of the cingulate cortex, was recorded during learning in all rabbits. Activity was also recorded in area 29 in the rabbits with area 24 lesions. Learning in rabbits with combined lesions was severely impaired and it was moderately retarded after lesions in area 24. MD thalamic and caudate training-induced neuronal discharge increments elicited by the CS+ were enhanced in rabbits with lesions, suggesting a suppressive influence of cingulate cortical projections on this activity. Early-, but not late-developing training-induced unit activity in area 29c/d was absent in rabbits with area 24 lesions, indicating that area 24 is a source of early-developing area 29 plasticity. These results are consistent with hypotheses of a theoretical working model, stating that: a) learning depends on the integrity of two functional systems, a mnemonic recency system comprised by circuitry involving area 24 and the MD nucleus and a mnemonic primacy system comprised by circuitry involving area 29 and the anterior thalamic nuclei; b) corticothalamic information flow in these systems suppresses thalamic CS elicited activity in trained rabbits; c) corticostriatal information flow is involved in avoidance response initiation. An absence of rhythmic theta-like neuronal bursts in area 29b in rabbits with area 24 lesions is attributable to passing fiber damage.

Animals↗
PubMed1990

Effects of concurrent manipulations of nicotinic and muscarinic receptors on spatial and passive avoidance learning.

The present study investigates the effects of concurrent manipulations of nicotinic and muscarinic cholinergic receptors on spatial and passive avoidance learning/retention in rats. Daily pretraining test injections of combinations of the subthreshold doses of muscarinic (scopolamine 0.3 mg/kg) and nicotinic (mecamylamine 2.5 mg/kg or 10 mg/kg) antagonists impaired acquisition of the water-maze task (WM). Drug-induced deficits were also observed during the retention trial: the groups injected with scopolamine 0.3 mg/kg, mecamylamine 10 mg/kg and scopolamine 0.3 mg/kg in combination with mecamylamine 2.5 mg/kg showed reduced spatial bias compared with controls. Single preretention test injections of the combination of subthreshold doses of mecamylamine (10 mg/kg) and scopolamine (0.8 mg/kg) impaired memory retrieval in WM. Combined pretraining injections of subthreshold doses of scopolamine (1.0 mg/kg) and mecamylamine (10 mg/kg) induced a severe passive avoidance impairment comparable to 2.0 mg/kg of scopolamine. However, preretention test injections did not impair passive avoidance retention. Either single or combined injections of hexamethonium (5.0 mg/kg, SC) and methylscopolamine (1.0 mg/kg) did not impair either passive avoidance or water-maze performance. The present results suggest that 1) nicotinic and muscarinic systems jointly modulate performance in spatial and avoidance learning tasks and 2) cholinergic antagonists affect acquisition functions more effectively than retention ability. These findings may be relevant to the clinical disorders, like Alzheimer's disease, which are associated with a loss of both cholinergic neurons and nicotinic receptors.

Animals↗
PubMed1979

Effect of p-chlorophenylalanine on avoidance learning of two differentially housed mouse strains.

The effect of p-chlorophenylalanine (PCPA) has been studied on the acquisition of avoidance learning and on brain concentrations of 5-hydroxytryptamine, 5-hydroxyindoleacetic acid and tryptophan of differentially housed male mice of Albino Swiss and DBA strains. The results obtained do not support the hypothesis that learning ability varies inversely with the concentration of brain 5-hydroxytryptamine. PCPA can appear as influencing learning ability of different strains of mice differentially housed, depending more on the emotional baseline of the animals than on brain 5-hydroxytryptamine modification.

5-Hydroxytryptophan↗
PubMed1989

Systemic injection of pirenzepine induces a deficit in passive avoidance learning in rats.

When injected IP, the M1 muscarinic receptor antagonist pirenzepine dose-dependently induced a deficit in passive avoidance learning in rats. This activity was optimal at 75 mg/kg injected 1 h before the acquisition session. The deficit induced by pirenzepine was antagonized by oxotremorine (0.03-0.3 mg/kg SC) and physostigmine (0.1 mg/kg SC), but not neostigmine. By comparison, under the same experimental conditions, physostigmine and oxotremorine also antagonized the deficit induced by an equipotent dose of scopolamine (0.5 mg/kg IP), although the activity of physostigmine appeared stronger against scopolamine than against pirenzepine. These results suggest that pirenzepine could produce a centrally-mediated behavioural disruption when injected systemically.

Animals↗
PubMed1977

Deficits in passive-avoidance learning following atropine in the developing rat.

The maturation of cholinergic inhibitory mechanisms that may be involved in passive-avoidance learning was studied in rats 14, 17, 21, 25, 28, and 34 days of age. Acquisition and extinction of the conditioned response were examined under saline and atropine sulfate (5 mg/kg). Learning was also tested following scopolamine hydrobromide injections (1, 4, 8 mg/kg) in rats 17 days of age and following alpha-methylatropine (5 mg/kg) in 17- and 34-day-old groups. In normal animals the rate of acquisition increased during ontogenesis, with a significant improvement between postnatal days 17 and 21, whereas the rate of extinction did not vary with age. Acquisition was impaired by atropine sulfate at all ages and even totally prevented in younger groups (14 and 17 days of age). It was also completely disrupted by scopolamine in 17-day-old rats. Extinction following acquisition under atropine was more rapid than after normal acquisition. Methyl-atropine was without effect. These results support the hypothesis of central cholinergic mechanisms involved in response suppression, already functioning in the rat 14 days of age and maturing mainly between the 17th and the 21st postnatal days.

Age Factors↗
PubMed1975

Methylphenidate effects on avoidance learning at two ages in the rat.

The major purpose of this investigation was to assess the effects of methylphenidate on avoidance learning at two ages. The subjects were 96 naive albino rats, equally divided between the sexes. One-half received daily drug administrations beginning at 47 days of age; one-half began at 87 days of age. Both groups were divided into three drug dosage levels (0.5, 1.5 and 4.5 mg/kg) and a distilled water control group. Methylphenidate was administered s.c. for a total of 18 days. Following 3 days of drug administrations only, 10 daily trials on avoidance conditioning were administered approximately 10 min after drugging to a total of 150 trials. The major findings indicated that: (1) no significant difference in avoidance response acquisition was obtained in the comparison between drug and control groups, (2) a dose effect was obtained in that the M4.5 group made siginificantly more correct responses than the M1.5 group, and (3) animals drugged beginning at 87 days made significantly more correct responses than those drugged beginning at 47 days.

Aging↗