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 91 records · Page 5Linked to original sources

PubMed1997

Effects of oxidative stress on the expression of limbic-specific protease neuropsin and avoidance learning in mice.

We evaluated the effects of oxidative stress in mouse brain induced by the intraperitoneal injection of diethyldithiocarbamate (DDC) on gene expression of the novel serine protease, neuropsin, and on shock-avoidance learning. The level of neuropsin mRNA in the hippocampal pyramidal neurons increased at 2 h after DDC treatment and decreased thereafter. At 7 days neuropsin mRNA significantly decreased to 60% of the pretreated control level and then returned to the control level at 30 days. Genes for tissue plasminogen activator, manganese superoxide dismutase, and heat shock protein did not differ in DDC-treated mice vs. the control group at 7 and 30 days. The shuttle-box avoidance learning was retarded at 7 days after DDC administration. However, it recovered to the control level at 30 days after DDC administration. The results suggest that generation of reactive oxygen species has an important role in neuropsin transcript in the limbic areas which might be related to the disturbance in avoidance learning.

Animals↗

PubMed1995

Effect of a composite Indian herbal preparation, CIHP(III) on avoidance learning during endurance performance of rats.

A nine week cross over study (5 weeks drug administration and 4 weeks withdrawal) was performed to see the effect of a composite Indian herbal preparation (CIHP III), viz. Mentat, on avoidance learning during endurance performance of albino rats. Runimex, a circular runway was used for this purpose. The number of stimuli viz. electrical shock of 10 mv, in drug treated rats at an oral dose of 47.86 mg/100 g body wt/single dose/day for 5 days were significantly reduced as compared to rats not taking any drug. The number of stimuli decreased significantly when the drug was started in the control group. No change in avoidance learning was observed over the period of 9 weeks in another group of rats. Results indicate significant improvement in avoidance learning during endurance performance due to the intake of CIHP(III).

Animals↗

PubMed1986

Exploration and avoidance learning after ibotenic acid and radio frequency lesions in the rat amygdala.

Open-field activity, avoidance behavior, and plasma corticosterone levels were studied after intraamygdala injections of 3.0 micrograms ibotenic acid (IBO) and radio-frequency (RF) lesions in the amygdala complex of male Wistar rats. The experiments were undertaken to evaluate the importance of amygdala neurons versus axons of passage in fear-motivated behavior. The IBO lesions led to increased open-field activity, but no impairments in active avoidance learning, nor changes in basal or experimental levels of plasma corticosterone. The RF lesions, on the other hand, led to an increase in experimental plasma corticosterone levels. In the one-way avoidance task the RF lesions, in contrast to the IBO lesions, led to significant impairments in the acquisition of the avoidance response. Although the long-term axon-sparing effect of IBO is questioned since cavities were detected in the affected areas 8 weeks after the injections, the differences in avoidance learning and in corticosterone levels between the RF and the IBO lesions indicate that the axons were functionally active at the time of testing (14-26 days postoperatively). The increase in open-field activity is attributed to the destruction of amygdala neurons and neurons in the overlying cortex, while an avoidance deficit seem to depend on the destruction of axons. On the basis of the behavioral results and the corticosterone data in these experiments, it is suggested that the behavioral changes are not attributable to a general reduction in the arousal of fear. However, since the IBO lesions did not affect the most medial parts of the amygdala complex including the central amygdala nucleus, the role of this nucleus in fear arousal has to be investigated further.

Amygdala↗

PubMed1988

Avoidance learning, Pavlovian conditioning, and the development of phobias.

This paper examines the role of Pavlovian conditioning in the acquisition, maintenance and elimination of human phobias. Because many conceptualizations of human fears and phobias are based on data from studies of avoidance learning in animals, we first review theories of avoidance. Our conclusion is that none of the extant theories provides an adequate account of avoidance learning, and we propose a model of avoidance that involves Pavlovian, but not instrumental learning. We then analyse critically arguments that Pavlovian conditioning plays only a small role in the aetiology of fears. Finally, the paper examines the implications of a conditioning model of avoidance for the study of human fears and phobias.

Animals↗

PubMed2000

Involvement of the medial precentral prefrontal cortex in memory consolidation for inhibitory avoidance learning in rats.

Adult male Wistar rats were trained in a step-down inhibitory avoidance learning task (3.0-s, 0.4-mA foot shock), received a 0.5-microl infusion of muscimol (0.02, 0.1, or 0.5 microg), AP5 (0.16, 0.34, 0. 5, 1.6, or 5.0 microg), SCH 23390 (0.05, 0.34, 0.5, or 1.75 microg), saline, or vehicle (DMSO 20%) into the anterior medial precentral area (Fr2) (CI) immediately after training, and were tested 24 h later. Muscimol (0.02, 0.1, or 0.5 microg), AP5 (0.34 or 0.5 microg), or SCH (0.5 or 1.75 microg) were amnesic. Then, animals were infused with muscimol (0.1 or 0.5 microg), AP5 (0.34, 0.5, or 5.0 microg), or SCH (0.5 microg) at other posttraining times and/or into the junction of Fr1-Fr2 (CII). Muscimol (0.1 and 0.5 microg) or SCH into CI were amnesic when given 90 or 180 min after training, but not when given 270 min after training. Muscimol (0.5 microg, but not 0.1 microg) or SCH into CII were amnesic when given 90 min after training, but not when given 0 or 180 min after training. AP5 (0.5, but not 5.0 microg) was amnesic when given into CI, but not into CII, at 0 or 180 min posttraining, and a trend toward an amnesic effect was seen at 90 min posttraining. The results suggest that 1) the glutamatergic, GABAergic, and dopaminergic systems in Fr2 are involved in the consolidation of memory for inhibitory avoidance learning, either directly or as parts of modulatory systems; and 2) timing of involvement of anterior Fr2 (CI) is different from that of posterior Fr2 (CII).

2-Amino-5-phosphonovalerate↗

PubMed1996

Interactive processing between glutamatergic and cholinergic systems involved in inhibitory avoidance learning of rats.

Rats were tested with a one-trial inhibitory avoidance paradigm in which the latency to enter the shock compartment served as a measure of memory retention. Pretraining administration of the non competitive NMDA receptor antagonist MK-801 (0.3 mg/kg i.p.) significantly reduced the response latency during the retention test given 24 h after rats received a step-through inhibitory avoidance training. MK-801 at 0.1 mg/kg did not affect the retention latency. The muscarinic receptor antagonist scopolamine (1.0 mg/kg i.p.) also interfered with the inhibitory avoidance response in the retention test when administered before the training trial. The lower dose of 0.3 mg/kg scopolamine, which by itself was ineffective, significantly impaired inhibitory avoidance learning when administered simultaneously with the behaviorally subthreshold dose of 0.1 mg/kg MK-801 before the training trial. These results suggest that interactive mechanisms regulated by concurrent activation of NMDA and muscarinic receptors are involved in learning processes of inhibitory avoidance performance in rats.

Animals↗

PubMed1994

Corticosteroid receptor antagonists are amnestic for passive avoidance learning in day-old chicks.

Glucocorticoids can modulate behavioural processes and neural plasticity. They are released during learning situations and can trigger neural actions through binding to brain receptors. We hypothesized that a glucocorticoid action could play a critical role in the mechanisms involved in long-term memory formation. In order to test this hypothesis, chicks were trained on a passive avoidance learning task and given bilateral intracerebral injections of selective mineralocorticoid (RU-28318) or glucocorticoid (RU-38486) receptor antagonists. The results showed that both antagonists alter information processing when injected prior to the training session. Possible state-dependent effects were discharged. Further experiments evaluating possible effects of the antagonists on concomitant aspects of the learning situation (such as novelty reaction and pecking pattern) indicated that, as opposed to the glucocorticoid receptor antagonist, the mineralocorticoid antagonist altered the birds' reactivity to non-specific aspects of the training task. These results suggest that the two types of intracellular corticosteroid receptors could be mediating different aspects of the information processing and storage involved in avoidance learning. In addition, this study points out that passive avoidance learning in the chick could be a good model to investigate the biochemical mechanisms involved in corticosteroid actions on learning-induced neural plasticity.

Amnesia↗

PubMed1994

Effect of caffeine and nicotine on avoidance learning in mice: lack of interaction.

Tested alone, nicotine (0.25 or 0.5 mg kg-1) improved shuttle-box avoidance learning in mice of the CD-1 strain. Caffeine had no effect at doses of 2.5 and 5 mg kg-1 and impaired performance at a dose of 10 mg kg-1. Combinations of the two drugs did not increase avoidance responses more than nicotine alone, nor was nicotine able to attenuate performance depression induced by the highest dose of caffeine. Lack of drug interaction in the avoidance test contrasts with the occurrence of interactive effects of the two drugs in a locomotor activity test. When given in combination, caffeine and nicotine increased locomotor activity at doses ineffective by themselves. The results seem to indicate no advantage in combining caffeine and nicotine to improve active avoidance learning.

Animals↗

PubMedDate not supplied

[The participation of the cholinergic systems of the dorsal and ventral striatum in the active avoidance learning of rats in a T maze].

Influence of cholinergic activation of dorsal (caudo-putamen) and ventral (accumbens) striatum on active avoidance learning was studied in chronic experiments in Sprague-Dawley male rats. The results obtained on the same behavioural model testify to specific roles of dorsal and ventral cholinergic systems in the control of motor behaviour. Single carbacholine microinjection into the right Accumbens increased the level of correct responses on the first and subsequent learning days. Similar microinjection into the left accumbens on the first training day improved the level of correct responses on the second and the third learning days. Microinjections into the dorsal striatum did not change active avoidance learning in T maze. Changes in locomotor activity of the animals of different experimental groups were principally of the same nature, i.e., the level of locomotor activity in the open field decreased from trial to trial in all the groups. Carbacholine microinjection did not change spontaneous locomotion in rats. However, there were variations in modifications of locomotor activity induced by microinjections into accumbens depending on localization of the cannula. Injection into the lateral accumbens induced the most pronounced changes. This fact testifies to the functional heterogeneity of this small nucleus.

Animals↗

PubMed2005

Involvement of neurotransmitters in urocortin-induced passive avoidance learning in mice.

The action of urocortin on one-way passive avoidance learning was tested in mice. Urocortin was administered into the lateral brain ventricle and the latency of the passive avoidance response was measured 24 h later. For study of the roles of various neurotransmitters in mediating the action of urocortin on the consolidation of memory, the animals were pretreated with different receptor antagonists. Urocortin facilitated the acquisition, consolidation and also retrieval of the passive avoidance response. The following receptor antagonists blocked the action of urocortin on consolidation: haloperidol, atropine, phenoxybenzamine, bicuculline, the CRF antagonist CRF9-41 and methysergide. Propranolol attenuated, but did not fully block the action of urocortin, while naloxone and nitro-L-arginine were ineffective. The results obtained demonstrate that urocortin is able to improve learning and memory and also retrieval processes in a passive avoidance learning in mice. D2, muscarinic cholinergic, alfa-adrenergic, CRF, serotonergic (5HT 1-2), GABA B receptors are involved in the consolidation of the passive avoidance response.

Adrenergic alpha-Antagonists↗

PubMed1996

[The characteristics of the effect of the rat neostriatal cholinergic system on normal active avoidance learning and in destruction of the intralaminar thalamic nuclei].

The learning of discriminative avoidance reflex in T-maze was studied on 57 Sprague-Dawley rats (divided into several experimental groups) at the normal conditions, both after carbacholine (0.03 mkg), or scopolamine (0.3 mkg) microinjections into neostriatum bilaterally, after uni- or bilateral lesions of intralaminar thalamic nucleus (Pf) and after neostriatal microinjections followed Pf lesion. It has been shown that bilateral carbacholine microinjections in neostriatum (in 4, 5 and 6 days of learning) significantly increased (p < 0.01) the level of correct realizations of discriminative avoidance reflex. Bilateral lesion of Pf resulted in irreversible destruction of preliminary learned active avoidance movement. In rats with preliminary lesion of Pf nuclei we had no possibility of learn discriminative avoidance reflex during 10 experimental days (160 trials). The neostriatal carbacholine microinjections to these animals didn't show any effect. It was concluded that intact afferent input from Pf nucleus is significant for activation of neostriatal neuronal background, necessary for cholinergic activation effect.

Animals↗

PubMed1990

Reward dominance and passive avoidance learning in adolescent psychopaths.

This study tests predictions that adolescent psychopaths are hyperresponsive to rewards (Quay, 1988) and deficient in passive avoidance learning (Newman & Kosson, 1986). Forty male adolescent juvenile offenders were divided into psychopaths and nonpsychopaths using cluster analysis. Subjects were administered a passive avoidance learning task which required learning when to respond to cards associated with either reward or punishment. Results showed a greater responsivity to reward in psychopaths, with no group differences in passive avoidance errors. Results lend support to the view that psychopaths tend to focus on the prospect of reward under conditions of mixed incentives and, when sufficiently motivated, are capable of improved performance. Together with findings of recent psychophysiological studies, these results suggest that adolescent psychopaths may have latent abilities which could have treatment implications.

Adolescent↗

PubMed1998

Progesterone facilitates the acquisition of avoidance learning and protects against subcortical neuronal death following prefrontal cortex ablation in the rat.

Following a cortical injury, neurons in areas near and connected to the site of injury begin to degenerate. The observed neuronal death may contribute to the severity of the observed behavioral impairments. The purpose of the present study was to examine if progesterone, a hormone known for its effectiveness at reducing cerebral edema, could protect against secondary neuronal death and facilitate the acquisition of an avoidance learning task in an ablation model of cortical injury. Rats served as sham controls or received bilateral ablation of the medial prefrontal cortex followed by a 10-day regimen of progesterone (4 mg/kg) or oil vehicle (1 ml/kg) beginning 1 h after cortical lesions. Progesterone-treated lesion rats showed a significant facilitation of avoidance learning compared to oil-treated lesion controls. In addition, progesterone-treated lesion animals did not differ from either progesterone- or oil-treated sham controls in avoidance learning. Anatomical analysis revealed that progesterone treatment decreased the amount of neuronal death seen in the striatum and the mediodorsal nucleus of the thalamus. The findings are consistent with the notion that progesterone is an effective neuroprotective agent and suggest that the hormone can reduce the behavioral impairments associated with frontal cortical ablation injury.

Animals↗

PubMed1988

Enhancement of passive avoidance learning through small doses of intra-amygdaloid physostigmine in the young rat. Its relation to the development of acetylcholinesterase.

Passive avoidance learning was studied in young rats 7-20 days old, in control conditions and after bilateral injections of physostigmine into the lateral amygdaloid nucleus. Acquisition in controls was possible from postnatal Day 8 on, progressed markedly after Day 11, and nearly reached maturity by Day 20. Physostigmine differentially altered acquisition depending on the dose: facilitation with low doses, no effect with moderate doses, and impairment with high doses. Enhanced learning through small doses of physostigmine was observed at all ages from Day 8 on, and was greater with 0.2 microgram than with 0.1 microgram. Maturation of the cholinergic innervation of the amygdaloid region was also studied between Days 9-20 using acetylcholine-esterase histochemistry. The results suggest that passive avoidance learning is dependent on amygdaloid cholinergic mechanisms early in life. In addition, very immature cholinergic systems, which are known to be uninfluenced by anticholinergic agents, react to anticholinesterases.

Acetylcholinesterase↗

PubMed2001

Endomorphins 1 and 2, endogenous mu-opioid receptor agonists, impair passive avoidance learning in mice.

The effects of intracerebroventricular administration of endomorphin-1 and endomorphin-2, endogenous mu-opioid receptor agonists, on passive avoidance learning associated with long-term memory were investigated in mice. Endomorphin-1 (10 and 17.5 microg) and endomorphin-2 (17.5 microg) produced a significant decrease in step-down latency in a passive avoidance learning task. beta-Funaltrexamine (5 microg) almost completely reversed the endomorphin-1 (17.5 microg)- and endomorphin-2 (17.5 microg)-induced shortening of step-down latency, although neither naltrindole (4 ng) nor nor-binaltorphimine (4 microg) produced any significant effects on the effects of endomorphins 1 and 2. These results suggest that endomorphins 1 and 2 impair long-term memory through the mediation of mu-opioid receptors in the brain.

Analgesics, Opioid↗

PubMed2006

NMDA receptor blockers prevents the facilitatory effects of post-training intra-dorsal hippocampal NMDA and physostigmine on memory retention of passive avoidance learning in rats.

In the present study, the effects of post-training intra-dorsal hippocampal (intra-CA1) injection of an N-methyl-D-aspartate (NMDA) receptor agonist and competitive or noncompetitive antagonists, on memory retention of passive avoidance learning was measured in the presence and absence of physostigmine in rats. Intra-CA1 administration of lower doses of the NMDA receptor agonist NMDA (10(-5) and 10(-4) microg/rat) did not affect memory retention, although the higher doses of the drug (10(-3), 10(-2) and 10(-1) microg/rat) increased memory retention. The greatest response was obtained with 10(-1) microg/rat of the drug. The different doses of the competitive NMDA receptor antagonist DL-AP5 (1, 3.2 and 10 microg/rat) and noncompetitive NMDA receptor antagonist MK-801 (0.5, 1 and 2 microg/rat) decreased memory retention in rats dose dependently. Both competitive and noncompetitive NMDA receptor antagonists reduced the effect of NMDA (10(-2) microg/rat). In another series of experiments, intra-CA1 injection of physostigmine (2, 3 and 4 microg/rat) improved memory retention. Post-training co-administration of lower doses of NMDA (10(-5) and 10(-4) microg/rat) and physostigmine (1 microg/rat), doses which were ineffective when given alone, significantly improved the retention latency. The competitive and noncompetitive NMDA receptor antagonists, DL-AP5 and MK-801, decreased the effect of physostigmine (2 microg/rat). Atropine decreased memory retention by itself and potentiated the response to DL-AP5 and MK-801. In conclusion, it seems that both NMDA and cholinergic systems not only play a part in the modulation of memory in the dorsal hippocampus of rats but also have demonstrated a complex interaction as well.

Analysis of Variance↗

PubMed1989

Place avoidance learning and stress-induced analgesia in the attacked mouse: role of endogenous opioids.

In this study, mechanisms of pain inhibition (tail-flick test) and memory (place avoidance paradigm) were investigated in attacked, DBA/2 and C57BL/6, mice. During training, exposure of test animals to 10 or 30 bites by an aggressive, isolated ICR mouse situated in the dark half of a bright/dark conditioning box induced a significantly higher social conflict analgesia in DBA than in C57 mice. Naltrexone (0.5 and 2.0 mg/kg) reduced this response in DBA mice that received 30, but not 10, bites and was ineffective in C57 mice. This points to different, opioid versus naltrexone-insensitive nonopioid, analgesic mechanisms. During place choice testing in the same box 24 h later, DBA mice that had received 30, but not 10, bites showed a significant, naltrexone-reversible, avoidance of the attack place. No place avoidance learning was observed in C57 mice. The data provided unequivocal evidence that place avoidance learning was a result of associative conditioning, in that neither pairing nor social conflict per se significantly changed the preference for the dark side seen in experimentally naive DBA mice. Antagonism of place avoidance conditioning was observed regardless of whether testing was carried out in the drugged or undrugged state, excluding possible state-dependent effects as an explanation for the naltrexone-induced impairment. Individual correlational analysis in saline-injected, attacked DBA mice revealed a negative relationship between the analgesic state immediately after training and the avoidance of attack place during testing. In summary, the results suggest strain-dependent analgesic and learning mechanisms and indicate that endogenous opioids released in attacked DBA mice support pain inhibition and modulate the memorization of attack place by their analgesic effects, as well as by mechanisms independent of pain inhibitory systems.

Animals↗

PubMed1977

One trial passive avoidance learning in neonatally hormone treated rats. Its relation with activity.

The performance in one trial passive avoidance learning and the degree of activity were determined in adulthood, from neonatal hormone treated and intact rats. Activity was measured in the same environmental conditions in which the learning test takes place, i.e., shuttle box unequally illuminated. The treated groups were androgenized females and castrated males. Intact groups were composed by normal males and females. Intact females showed more activity than intact males. Castrated males and androgenized females displayed a degree of activity similar to the normal females. This score was negatively correlated with the total time that each animal remained in the dark compartment of the box. In this respect the normal males showed greater dark preference than the other three groups, which had no differences among them. Similar results to that of dark preference were obtained in performance on one trial passive avoidance learning, that is, androgenization in females did not produce a significant effect in this test and castration in males decreased their performance. A linear correlation between activity and passive avoidance score could be established.

Animals↗