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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↗
PubMed1969

Avoidance learning: long-lasting deficits after temporal lobe seizure.

Microinjections of carbachol (carbamylcholine chloride) into the amygdaloid complex of rats produced behavioral and electrophysiological seizures which subsided within 24 hours. A persisting functional change caused a deficit in avoidance learning 1 to 3 weeks after the seizure. A cholinergic system is implicated by the fact that cholinergic blockade (scopolamine) of the amygdala during training reversed the effects of the seizures induced by carbachol.

Amygdala↗
PubMed1993

Strain-dependent effects of gamma-L-glutamyl-L-aspartate, a NMDA antagonist, on retention of a Y-maze avoidance learning task in mice.

The NMDA receptor antagonist, gamma-L-glutamyl-L-aspartate (gamma-LGLA), suppressed spontaneous improvement in posttraining performance in Swiss mice during the hours following acquisition of a Y-maze avoidance learning task. Since variability in posttraining performance is at least partially due to genetic factors, we compared the effects of gamma-LGLA on retention of Y-maze learning in C57BL/6J, DBA/2J and BALB/c mice. Mice had to leave the start alley of the maze within the first 5 s (temporal component) and to choose the left alley (spatial component). C57BL mice significantly improved their performance from 1 h to 24 h posttraining, whereas DBA/2J and BALB/c mice did not. However, only retention of the temporal component improved over time in C57BL. gamma-LGLA administered immediately posttraining (0.025-25 mumol/kg, i.p.) dose-dependently impaired retention of the temporal component in C57BL mice 48 h later, but had no significant effect on retention of the spatial component. gamma-LGLA administered 24 h posttraining induced a similar but weaker deficit. In contrast, gamma-LGLA did not significantly affect retention of DBA/2J and BALB/c mice, regardless of the component analyzed or the time of administration. It had no effect on locomotor activity or emotional reactivity of animals of any strain. These results support the hypothesis of a specific action of gamma-LGLA on mechanisms involved in the treatment of information during the hours following acquisition, and suggest that NMDA receptors are involved in this action.

Animals↗
PubMed1992

Passive avoidance learning in the young chick results in time- and locus-specific elevations of alpha-tubulin immunoreactivity.

A monoclonal antibody was used to examine changes in immunoreactivity of the cytoskeletal protein, alpha-tubulin, following passive avoidance learning in day-old chicks. Postmitochondrial fractions (16,000 g supernatants) were prepared from specific forebrain loci taken at several time points after training and assayed with the anti-alpha-tubulin antibody, YL1/2. Of the regions examined, elevations in the titre of YL1/2 were found in the left intermediate hyperstriatum ventrale 1 h, 6 h and 24 h following training, in the left lobus parolfactorius 1 h following training and in the right lobus parolfactorius 6 h and 24 h following training. No training-related changes were detected in a third forebrain region, the paleostriatum augmentatum. These results regarding the cellular dynamics of memory formation in the chick confirm and expand on earlier findings from our laboratory.

Animals↗
PubMed1995

Effects of (-)-S-2,8-dimethyl-3-methylene-1-oxa-8-azaspiro[4,5]decane L-tartrate monohydrate (YM796), a novel muscarinic agonist, on disturbance of passive avoidance learning behavior in drug-treated and senescence-accelerated mice.

Effects of YM796 (-)-S-2,8-dimethyl-3-methylene-1-oxa-8-azaspiro[4,5]decane L-tartrate monohydrate; a novel muscarinic agonist, were observed on disturbance of passive avoidance learning behavior in drug- (protein synthesis inhibitor and anticholinergic drugs) treated and senescence-accelerated mice in comparison with those of a muscarinic agonist (AF102B) and acetylcholinesterase inhibitors (E2020 (1-benzyl-4-[(5,6-dimethoxy-1-indanone-2-yl) methyl] piperidene hydrochloride), NIK247 [9-amino-2,3,5,6,7,8-hexahydro-1H-cyclopenta(b)-quinoline monohydrate hydrochloride], THA (9-amino-1,2,3,4-tetrahydroacridine) and physostigmine). All tested drugs administered before training significantly prolonged the shortened latency of step-through induced by the protein synthesis inhibitor cycloheximide (150 mg/kg s.c.). This shortened latency was also significantly prolonged when YM796 was administered immediately after training, but not when administered before the test trial. The ameliorating effect of YM796 on the impairment in learning behavior by cycloheximide was significantly suppressed by pirenzepine (0.1 micrograms/mouse i.c.v.). When administered before training, all test drugs prolonged the shortened latency of step-through induced by treatment with the anticholinergic drugs [scopolamine (1 mg/kg s.c.) and hemicholinium-3 (0.3 microgram/mouse i.c.v.)], suggesting that they ameliorated the impairment of learning behavior. This shortened latency in scopolamine-treated mice was also significantly prolonged by YM796, AF102B, E2020, NIK247 and physostigmine when administered immediately after training, but not when administered before the test trial. The pharmacological actions of YM796 administered immediately after training and before the test trial in hemicholinium-3-treated mice were similar to those in scopolamine-treated mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗