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 163 records · Page 9Linked to original sources

PubMed1997

Inhibitory avoidance learning alters the amygdala calcium/calmodulin-dependent protein kinase II activity in rats.

This study investigated the role of amygdala CaM-kinase II (calcium/calmodulin-dependent protein kinase II) in affective learning and memory. In Experiment I, two groups of rats were trained on a one-trial step through inhibitory avoidance learning task. The experimental group received a high intensity foot shock contingent upon the stepping-through behavior, whereas the control group received a series of non-contingent low intensity foot shock during training. The experimental rats showed significantly higher retention scores than the control rats. Correspondingly, rats in the experimental group showed significantly higher Ca2+-independent activity of CaM-kinase II than the controls. Intra-amygdala injection of a specific CaM-kinase II inhibitor, KN-62, before the training trial disrupted affective learning. In comparison with the vehicle-injected controls, pretraining injection of KN-62 impaired the acquisition of affective specific learning. These results, taken together, indicated that the activation of amygdala CaM-kinase II in the amygdala is associated with the affective learning behavior, and may be one of the neural mechanisms underlying formation of affective memory.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1998

Observation learning in day-old chicks using a one-trial passive avoidance learning paradigm.

We tested the hypothesis that day-old chicks, Gallus gallus domesticus, can learn to avoid an aversive stimulus if they observe the responses of another chick. In experiment 1, one of a pair of chicks (the actor) was allowed to peck at a bead coated in the bitter-tasting substance methylanthranilate (MeA), while we prevented the other chick (the observer) from pecking the bitter-tasting bead by separating the chicks with a piece of wire mesh. Both chicks avoided pecking at a similar but dry bead 0.5, 3 and 24 h after the observer chick saw the actor chick peck at an MeA-coated bead. By contrast, when the actor chick had pecked at a water-coated bead, both chicks continued to peck at a dry bead at 0.5, 3 and 24 h after training. Experiment 2 investigated whether observer chicks showed avoidance if they were prevented (by the insertion of an opaque barrier) from observing their companion pecking at the MeA-coated bead during either training or testing. Observer chicks that could not see their companion during training but could observe the actor chicks at test showed no subsequent avoidance whereas chicks that observed the actor chick at training, but not during testing, showed high levels of avoidance. Although the sensory cues (visual, auditory or olfactory) or types of behaviour (i.e. levels of pecking or head shaking) that the observer chick used to maintain avoidance remain unclear, the results show that chicks can learn about an aversive object by observing the responses of a conspecific. (c) 1998 The Association for the Study of Animal Behaviour.

Journal Article↗

PubMed1993

Effects of indeloxazine hydrochloride, a cerebral activator, on passive avoidance learning impaired by disruption of cholinergic transmission in rats.

The effect of indeloxazine [(+/-)-2-[(inden-7-yloxy)methyl]morpholine hydrochloride, YM-08054], a cerebral activator, on passive avoidance learning by disruption of cholinergic transmission was investigated in rats. Indeloxazine prolonged the latency for stepping out of an illuminated compartment into a dark compartment, in both mature and aged rats. Disruption of cholinergic transmission was induced by injection of scopolamine, ethylcholine, treatment with aridinium ion (AF64A) and by lesioning the nucleus basalis magnocellularis. The shortened latency in these models was prolonged when indeloxazine was administered before training in doses which did not affect spontaneous movement or the response to pain in mature rats and administration of indeloxazine, immediately after training, also had an ameliorating effect on passive avoidance in the lesioned rats. In biochemical studies, indeloxazine increased the extracellular concentration of acetylcholine in the frontal cortex of mature rats. These results suggest that indeloxazine possesses facilitatory effects on cerebral function, in part due to activation of the central cholinergic system.

Acetylcholine↗

PubMed1997

Long-lasting mnemotropic effect of substance P and its N-terminal fragment (SP1-7) on avoidance learning.

We investigated the long-lasting effect of peripheral injection of the neuropeptide substance P (SP) and of some N- or C-terminal SP fragments (SPN and SPC, respectively) on retention test performance of avoidance learning. Male Wistar rats (220 to 280 g) were trained in an inhibitory step-down avoidance task and tested 24 h or 21 days later. Immediately after the training trial rats received an intraperitoneal injection of SP (50 micrograms/kg), SPN 1-7 (167 micrograms/kg) or SPC 7-11 (134 micrograms/kg). Control groups were injected with vehicle or SP 5 h after the training trial. The immediate post-training administration of SP and SPN, but not SPC, facilitated avoidance behavior in rats tested 24 h or 21 days later, i.e., the retention test latencies of the SP and SPN groups were significantly longer (P < 0.05, Mann-Whitney U-test) during both training-test intervals. These observations suggest that the memory-enhancing effect of SP is long-lasting and that the amino acid sequence responsible for this effect is encoded by its N-terminal part.

Animals↗

PubMedDate not supplied

[The long-term effect of acute hypoxic hypoxia on shuttlebox avoidance learning in rats].

Long-term influence was studied of the acute hypoxic hypoxia seance on rats behaviour in situation of elaboration of the conditioned reaction of active avoidance of electric shocks in shuttle chamber. It was found that in 2.5-3 months after the hypoxia seance, the experimental animals significantly differed from the intact controls by dynamics of CR elaboration (rats which had hypoxia were ahead of the control ones) and by distribution of the conditioned reactions latencies (for experimental animals this distribution was shifted to minor values). The character of these behavioural shifts coincided with that observed in the group of rats with local unilateral hippocampus lesion. The obtained results and numerous data presented in literature on the influence of the hippocampus lesion on animals shuttle avoidance learning, allow to conclude that the seance of hypoxic hypoxia leads to the disturbance of the hippocampus function. This conclusion conforms to the data on diffusive death of the hippocampal and neocortical neurones as a result of hypoxia action.

Acute Disease↗

PubMed2000

Cytochemical characteristics of the brain in rats differing in active avoidance learning ability.

Brain structures were examined in two mouse strains differing in active avoidance learning in a shuttle box. Protein content and concentration, area of the cytoplasm and nuclei of neuron in layers III and V of the sensorimotor cortex were higher in rats with high learning ability. The detected morphochemical differences between the same brain structures of rats with high and low learning capacity can be attributed to this capacity.

Animals↗

PubMed2000

Consolidation of passive avoidance learning is associated with transient increases of polysialylated neurons in layer II of the rat medial temporal cortex.

Within the rat medial temporal lobe, transient modulations of neural cell adhesion molecule (NCAM) polysialylation have been observed to follow spatial learning. These have been attributed to neuroplastic events associated with the processing of information destined for long term memory consolidation. To determine if similar events are associated with avoidance learning, we investigated change in polysialylated cell number in the entorhinal, perirhinal, and piriform cortex, following acquisition of a passive avoidance task in the rat. Direct quantification of polysialylated neurons in layer II of these cortical regions revealed a significant increase in polysialylated cell frequency at 12 h following passive avoidance training. Unlike spatial learning, the increased expression of polysialylated neurons persisted for up to 24-48 h following training. In the more dorsal aspect of the perirhinal/entorhinal cortex, this increase was found to be specific to learning, as it was not observed in animals rendered amnesic with scopolamine. By contrast, change in polysialylated cell frequency in the ventral aspect of the medial temporal lobe was only partially reduced by amnesic doses of scopolamine. The persisting activation of NCAM polysialylation in the more dorsal aspects of the perirhinal and entorhinal cortex is suggested to reflect the need for more extensive synaptic alterations, as compared to those required for the consolidation of spatial learning. Moreover, the neuroplastic modulations observed in the more ventral regions of the entorhinal and perirhinal cortex appear to be a unique aspect of avoidance conditioning that reflects the activation of alternative learning strategies associated with motivational and/or contextual parameters of the task.

Animals↗

PubMed1977

Effects of methylphenidate on avoidance learning in the aged rat.

Twenty Sprague Dawley rats, aged 22 to 26 months were given subcutaneous injections of 4.5 mg/kg methylphenidate or distilled water. Twelve minutes after the single injection was given, rats began 90 trials of avoidance conditioning. Drug animals made significantly more correct responses than did the control animals. tresults indicate that use of methylphenidate in aged rats improved avoidance learning.

Aging↗

PubMed2001

Effects of intrahippocampal aniracetam treatment on Y-maze avoidance learning performance and behavioral long-term potentiation in dentate gyrus in rat.

Effects of intrahippocampal treatment of aniracetam, a selective agonist for DL-alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproionic acid (AMPA) receptors, on Y-maze avoidance learning task and behavioral long-term potentiation (LTP) in perforant path-dentate gyrus were studied in freely moving rats by using in vivo electrophysiology combined with behavioral tests. The results were as follows: (1) intrahippocampal treatment of aniracetam reversibly enhanced basal synaptic transmission in perforant path to dentate gyrus in a dosage dependent manner; (2) aniracetam produced improvement in Y-maze learning performance when administration occurred 5 min prior to maze learning; (3) aniracetam administration significantly facilitated behavioral LTP in dentate gyrus, while the maximal amplitude of LTP has no significant difference when compared to saline group. The present results indicate that hippocampal AMPA receptors are involved in learning and memory.

Animals↗

PubMed1991

The NMDA receptor antagonists, CPP and gamma-L-glutamyl-L-aspartate, selectively block post-training improvement of performance in a Y-maze avoidance learning task.

Behavioral effects of CCP and gamma-L-glutamyl-L-aspartate (gamma-LGLA) were studied in a Y-maze avoidance learning task. Male Swiss mice had to leave the start alley of the maze within the first 5 s of a trial (temporal component) and to choose the left alley (spatial component) to avoid footshocks; they were trained to a criterion of 7 correct out of 8 consecutive trials. CPP and gamma-LGLA when administered immediately following the learning session (0.025-200 mumol/kg, i.p.) significantly impaired retention 48 h later at doses of 0.025-0.25 and 0.25-25 mumol/kg, respectively, but had no significant effect at higher doses. CPP, when administered 30 min before the learning session (0.025-25 mumol/kg) did not affect learning acquisition at any dose, whereas it significantly impaired retention 48 h later but only at the doses of 0.025-0.25 mumol/kg. CPP and gamma-LGLA did not erase all memory traces; posttraining performances on the temporal component, which significantly improved in control animals during the hours following acquisition, were much more affected by CPP and gamma-LGLA than posttraining performances on the spatial component which did not improve over time in controls. Moreover, CPP (0.025-25 mumol/kg) had no effect on spatial recognition memory in an alternation task in which no spontaneous improvement of posttraining performance was observed in controls. These results strongly suggest that CPP and gamma-LGLA interfere with mechanisms underlying posttraining organization of memory traces and that NMDA receptors are involved in this action.

Animals↗

PubMed1979

Impairment by apomorphine of one-trial passive avoidance learning in mice: the opposing roles of the dopamine and noradrenaline systems.

Pretraining administration of the dopaminergic stimulant apomorphine (0.25--16 mg/kg) impaired retention performance of mice on a one-trial passive avoidance task. Only with a very high dose (16 mg/kg) of this drug did the effect seem related to an interference with memory formation processes. Of the dopamine receptor-blocking agents used, haloperidol (0.125--1 mg/kg), but not chlorpromazine or clozapine (0.25--4 mg/kg), prevented the apomorphine effect. Phenoxybenzamine (8 mg/kg), a noradrenaline receptor-blocker, antagonized the haloperidol effect and, when combined with a subeffective dose of apomorphine, impaired passive avoidance learning. The results obtained are interpreted in terms of the proposed inhibitory actions exerted by central noradrenaline on dopamine systems of the brain.

Animals↗

PubMed2002

Effects of intrahippocampal injection of GABAergic drugs on memory retention of passive avoidance learning in rats.

The effect of post-training intrahippocampal injection of gamma-aminobutyric acid (GABA) receptor agonists and antagonists, immediately after a training session on memory retention of passive avoidance learning in rats, was measured in the presence and absence of physostigmine. Post-training treatments were carried out in all the experiments. The different doses of the GABAA receptor agonist muscimol (2, 4 and 6 microg/rat) decreased memory retention in rats dose-dependently. The higher response was obtained with 6 microg/rat of the drug. When the GABAA receptor antagonist bicuculline (0.5, 1, 2 and 4 microg/rat) was administered, only one dose of the drug (1 microg/rat) increased memory retention; however, the antagonist reduced the effect of muscimol. The GABAB receptor agonist, baclofen (0.25, 0.5, 1 and 2 microg/rat) also reduced memory retention in the animals. Intrahippocampal injection of lower doses of the GABAB receptor antagonist CGP35348 (P-[3-aminopropyl]-p-diethoxymethyl-phosphinic acid) (2.5, 5, 10 microg/rat) did not effect memory retention, although the higher doses of the drug (25 and 50 microg/rat) decreased memory retention. The doses of antagonist (2.5, 5 and 10 microg/rat), which did not elicit any response alone, reduced the effect of baclofen. The inhibitory response of CGP35348 was also decreased by bicuculline. In another series of experiments, physostigmine improved memory retention. The GABA receptor agonists, muscimol and baclofen, as well as the GABA receptor antagonists bicuculline and CGP35348, decreased the effect of physostigmine. Atropine decreased memory retention by itself and potentiated the response of muscimol and baclofen. It is concluded that GABAA and GABAB receptor activation may be involved in the impairment of memory retention.

Animals↗

PubMed1997

Uncompetitive NMDA receptor antagonists attenuate NMDA-induced impairment of passive avoidance learning and LTP.

In general, N-methyl-D-aspartate (NMDA) receptor antagonists inhibit learning and long term potentiation (LTP). However, it has been suggested that direct tonic, i.e. non-temporal, activation of NMDA receptors, in contrast to learning, may lead to an increase in synaptic "noise" and, in turn, to a loss of association detection. In the present study, a two-choice passive avoidance task and LTP in vitro (CA1 hippocampal region) were used to address this issue. Dark avoidance learning was impaired by systemic NMDA administration (starting at 25 mg/kg) that was not related to either toxic effects or state-dependent learning. NMDA-induced amnesia was antagonized by ((+)-5-methyl-10,11-dihydro-5H-dibenzocyclohepten-5,10-imine maleate (MK-801) and 1-amino-3,5-dimethyladamantane (memantine), starting at low doses of 0.05 and 2.5 mg/kg, respectively, in a bell-shaped dose-response relationship. A competitive NMDA receptor antagonist CGP-39551 failed to reverse NMDA-induced amnesia. In hippocampal slices, NMDA (10 microM) depressed (S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolproprionic acid (AMPA) receptor-mediated field potentials in CA1 and also caused a moderate reduction of LTP induction/expression. It was this latter effect that was antagonized by memantine (1 microM). Thus, under conditions of tonic activation of NMDA receptors, uncompetitive NMDA receptor antagonists can paradoxically reverse deficits in learning and synaptic plasticity.

2-Amino-5-phosphonovalerate↗

PubMed1978

Central catecholamine and peripheral noradrenaline depletion by 6-hydroxydopamine and active avoidance learning in rats.

Three experiments are reported on the relation among catecholamine (CA) depletion, plasma corticosterone (11-OHCS) levels, and active aversive learning. A baseline study showed no significant relation beteen resting levels of 11-OHCS and central and/or peripheral CA depletion. On a two-way avoidance learning task, depletion of brain CAs produced a widespread learning deficit. When both central and peripheral CAs were depleted, only escape learning emerged. Similar effects occurred on a one-way task, but differences were not so marked. The findings are discussed in terms of a theory of CA-dependent cues.

11-Hydroxycorticosteroids↗

PubMed1976

Chronic intermittent ethyl alcohol inhalation and avoidance learning.

Weanling male and female rats were chronically exposed to alcohol for 50 days using an intermittent inhalation technique which does not cause alcohol dependency. After 17 days of no exposure to alcohol, animals began two-way active avoidance testing. Results indicated that males were impaired on this task and females were not while at the same time males had reduced body weights. The male weight reduction was not responsible for the avoidance impairment. It was concluded that impaired avoidance learning following chronic esposure to alcohol is not specific to dependency models of animal alcoholism.

Aerosols↗

PubMed1994

[Response types to shock and avoidance learning in inbred strains of mice].

The effects of shock intensity on response types to shock (Experiment 1) and the relationship between response types and avoidance learning (Experiment 2) were investigated in four inbred strains of mice (BALB/c, C3H/He, C57BL/6 and DBA/2J). In Experiment 1, mice received a one-second inescapable shock, which ranged in intensity from .01 to .4 mA (12 levels). Response types to shock were observed, and locomotion increased in all strains as the shock intensity increased. Additionally, the C3H/He strain also increased jumping response at shocks greater than .2 mA. In Experiment 2, the four strains were trained for shuttle avoidance with three shock intensities (.06, .16 and .4 mA). Two responses, locomotion into the adjacent compartment (L-typed) and rearing or jumping (R-typed), were equally effective in terminating the shock. While all strains learned the task at all the levels of shock intensities, the performance of the BALB/c strain declined as the intensity decreased. BALB/c and C57BL/6 strains avoided the shocks mainly by L-typed response across all the intensities. Likewise, the DBA/2J strain predominately displayed L-typed responses, but some R-typed responses did occur. The C3H/He strain, on the other hand, largely avoided the shocks by the R-typed response, especially in the .06 and .4 mA conditions.

Animals↗

PubMedDate not supplied

Avoidance learning in rats devoid of the telencephalon plus thalamus.

Two experiments were undertaken to investigate whether learning of an inhibitory avoidance response is possible in rats devoid of the whole forebrain, except for the hypothalamus. In experiment I all telencephalic structures were surgically ablated. Twenty-four hours later the rats were given a learning trial in the up-hill avoidance task. When tested 2 h later, the animals given a tail-shock contingent on the up-hill response showed significant increases in step-up latencies in comparison with control groups that had received non-contingent shock or no shock. In experiment II the thalamus was removed in addition to the telencephalon. As in experiment I, the animals received either tail-shock contingent on the up-hill reaction, no tail-shock, or non-contingent shock. When tested 2 and 24 h after the training, the animals that had received response-contingent shock showed significant increases in latencies to ascend the platform. These results indicate that inhibitory avoidance conditioning is still possible in rats devoid of the telencephalon plus thalamus.

Animals↗

PubMed1983

Effect of propranolol treatment in pregnant rats on motor activity and avoidance learning of the offspring.

Rats born to mothers treated with propranolol, during days 8-22 of gestation, displayed hyperactivity in the open field which lasted up to 60 days of age and an impairment of avoidance in the shuttle box which was more marked in the male rats. Females exhibited hyperactivity in the open field but developed impaired avoidance learning only when exposed prenatally to both propranolol and hypoxia. Propranolol administration during the last term of pregnancy (days 18-22) affected mostly shuttle box performance. In contrast, hyperactivity could be induced by treatment during various stages of pregnancy, (days 8-22, 8-18, or 18-22) with the duration of hyperactivity being directly related to the length of treatment of the mothers. The possible mechanism of the disruptive effect of propranolol in the fetus and newborn is discussed.

Aging↗