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PubMed1991

[Changes in oxygen metabolism during active avoidance learning in spontaneously hypertensive and normotensive rats].

A decreased pO2 was found in the SHR rats' sensomotor area of the brain cortex in resting as well as in learning of the avoidance reflex as compared with the WKY rats. Avoidance training resulted in the decrease of pO2 in the brain tissue and the increase of common oxygen consumption. The recovery of common oxygen consumption to initial level took longer in the SHR rats. The number of the avoidance conditioned responses was greater in the SHR rats than in the WKY ones. The changes of the SHR rats' oxygen metabolism seem to be caused by morphological alterations, resulting in the peculiarities of the avoidance behaviour formation. These changes are enhanced in ageing and most obvious under emotional-motor loads in hypertensive animals.

Aging↗
PubMed1984

Temporal changes in avoidance learning in physically alcohol-dependent rats following withdrawal.

The effects of post withdrawal periods over a range of 0 to 48 hours on avoidance learning in physically alcohol-dependent rats were examined in a shuttle-box situation. Liquid diet containing 5% ethyl alcohol was withdrawn after 15 days. The severity of the alcohol withdrawal syndrome in rats changed with time elapsed after withdrawal. Severe withdrawal syndrome such as increase in failure to escape from shock due to convulsion, increase in intertrial responses due to hyperactivity, and death appeared when the test was started 4.5 hours after withdrawal. On the other hand, avoidance learning was reduced almost zero within 24 hours, but it recovered to a normal level 48 hours after withdrawal of alcohol.

Animals↗
PubMed2000

Immunohistochemical estimation of rat brain somatostatin on avoidance learning impairment induced by thiamine deficiency.

In rats, on the 25th day after the start of a thiamine-deficient (TD) diet, impairment of avoidance learning was significantly induced in proportion to the decrease somatostatin (SST) fluorescence intensity in the cortex, amygdala, thalamus, hypothalamus, and hippocampus, including the CA1, CA2, and dentate gyrus (DG). Only a single injection of thiamine HCl (0.5 mg/rat, subcutaneous) on the 14th day after the start of a TD diet improved the amnesia to the level of the pair-fed control and prevented the decrease in the SST level. Whereas these reversal effects of thiamine treatment were not found when the treatment was given on the 21st day after the start of a TD diet. These results indicate that, after a certain degree of thiamine deficiency, TD-induced behavioral effects might be reversible, but some neuronal fibers might be irreversibly damaged, probably due to the reduction of thiamine-dependent enzymes in brain mitochondria. The results also suggest the possibility that SST in the brain may be closely related to the avoidance learning impairment induced by TD.

Animals↗
PubMed1976

The effect of diethyldithiocarbamate on passive avoidance learning by chicks (Gallus domesticus).

Diethyldithiocarbamate (DDC), a competitive inhibitor of dopamine-B-hydroxylase, produced a dosage-related depletion of neural NE and impairment of passive avoidance learning in young chicks. Retention was not impaired, however, as shown by normal relearning of the task a day later, when the drug was no longer active. Perhaps, neural NE depletion impairs ability to inhibit responding and, thus, impairs passive or inhibitory avoidance learning indirectly. Alternatively, NE depletion may slow down learning by interfering with consolidation, but if the task is well learned, it is remembered.

Animals↗
PubMed1996

Neural substrates of discriminative avoidance learning and classical eyeblink conditioning in rabbits: a double dissociation.

In a previous study, lesions of the deep cerebellar nuclei blocked classical eyeblink conditioning, but did not impair discriminative avoidance learning in rabbits. Here, was also found previously, lesions of the anterior and medial dorsal thalamic nuclei severely impaired discriminative avoidance learning. However, these lesions had no impact on discriminative eyeblink conditioning or reversal learning. These results complete the demonstration of a double dissociation, indicating distinct neural substrates for the acquisition of these learned behaviors. It is proposed that the two learning circuits identified by these studies mediate, respectively, acquisition of specific adaptive reflexes and whole-body, voluntary goal-directed movements.

Animals↗
PubMed2003

Lipopolysaccharide induces biochemical alterations in chicks trained on the passive avoidance learning task.

We have recently shown that activation of the immune system with lipopolysaccharide (LPS) results in memory-processing deficits for the passive avoidance learning task in the day-old chick. The current study examined two important issues in understanding the mechanisms underlying these memory deficits associated with immune system activation, namely, whether LPS (1) impairs Na(+)/K(+)-ATPase functioning and (2) increases corticosterone (CORT) concentrations in chicks trained on the task. As the effects of LPS on sickness behavior have only previously been characterized in older chickens, this study also tested whether LPS is able to produce similar alterations in day-old chicks. LPS decreased brain Na(+)/K(+)-ATPase activity and increased plasma concentrations of CORT in chicks trained on the passive avoidance learning task. These findings give an insight into some of the mechanisms that may be responsible for the LPS-induced memory-processing deficits. Consistent with previous research in older chickens, LPS increased body temperature in a dose-dependent manner, however, only the lowest dose of LPS tested significantly decreased food intake in the day-old chicks.

Animals↗
PubMed1984

Implication of amygdaloid muscarinic cholinergic mechanisms in passive avoidance learning in the developing rat.

Young rats, 12-20 days of age, received bilateral microinjections of atropine sulfate (1, 5 and 20 micrograms) into the basolateral part of the amygdala, and were trained to learn a cool-draft-stimulus passive avoidance task 17 min later. Twelve-day rats did not perform differently from their controls. In contrast, rats 13-20 days of age exhibited significant age- and dose-related acquisition deficits. Sensitivity to atropine was high until day 17, and decreased progressively thereafter. These results demonstrate that muscarinic cholinergic synaptic elements located in the basolateral part of the amygdala are involved in passive avoidance learning in the young rat and begin to function on postnatal day 13. They also suggest that the number of functioning muscarinic receptor sites increase reliably after day 17.

Amygdala↗
PubMed1992

Effects of dopamine receptor agonists on passive avoidance learning in mice: interaction of dopamine D1 and D2 receptors.

The present study examined the effects of dopamine D1 and D2 receptor agonists on the acquisition stage of passive avoidance learning and on locomotor activity in mice. The D2 agonist, RU 24213 (1-10 mg/kg s.c.), and the non-selective agonist, apomorphine (0.3-3 mg/kg s.c.), but not the D1 agonist, SKF 38393 (1-10 mg/kg s.c.), impaired learning and activated locomotion. RU 24213 (1 mg/kg s.c.) was more effective in impairing learning than in activating locomotion. The concurrent administration of SKF 38393 (10 mg/kg i.p.) and RU 24213 (1 and 3 mg/kg s.c.) produced a synergistic effect in both behavioral situations. The D1 antagonist, SCH 23390 (0.025 mg/kg i.p.), slightly inhibited the effects of apomorphine and of the combination of SKF 38393 and RU 24213 on learning but not on locomotion. The D2 antagonist, (-)-sulpiride (40 mg/kg i.p.), completely blocked these effects in both situations. These results suggest that dopamine receptor agonists impair passive avoidance learning through the D2 receptor, and that D1 and D2 receptors act synergistically in this impairment, as they do in their effects on locomotion. The involvement of D1 and D2 receptors is qualitatively similar in each of these behaviors, although some small differences may exist.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1995

The pentadecapeptide [Ser1]histogranin impairs passive avoidance learning in mice.

The peptides, histogranin and [Ser1]histogranin, were recently shown to modulate NMDA receptor function. In the present study, the effects of intracerebroventricular (i.c.v.) administration of [Ser1]histogranin and of the histogranin receptor antagonist, histogranin-(1-10), were examined on step-down type passive avoidance learning in mice. [Ser1]Histogranin (30-60 nmol) impaired retention, after post-training administration, but not when it was administered just prior to the retention assay. Histogranin-(1-10) (60 nmol) facilitated learning during training, without affecting retention. Co-administration of histogranin-(1-10) with [Ser1]histogranin (60 nmol each) led to a significant prevention of [Ser1]histogranin-induced learning impairment. These results indicate that [Ser1]histogranin impairs passive avoidance learning according to the pattern of NMDA receptor antagonists and involving specific histogranin sites.

Animals↗
PubMed2003

Selection for differences in avoidance learning: the Syracuse strains differ in anxiety, not learning ability.

In this review the derivation of the Syracuse (SHA/Bru and SLA/Bru) strains of hooded rats that were selectively bred for differences in active two-way shuttle-box avoidance learning is described, together with a summary of the behavioral, hormonal, anatomical, physiological, and pharmacological characteristics that covary with the realized phenotypes. A selective genetic analysis is also described, which indicates that all of the five assessed covariates cosegregate with the avoidance phenotypes and are, therefore, closely linked to the high- and low-avoidance genotypes, which also suggests that a relatively few closely linked genes underlie the realized phenotypes. The low-avoidance phenotype seems best characterized in terms of high levels of state/trait anxiety, whereas the reverse is true of the high-avoidance phenotype. Anomalous endocrine data seem not to be consistent with the behavioral interpretation and remain to be resolved. However, it also seems clear that having selected for a difference in avoidance learning, the realized phenotypes do not involve the fundamental neurobiological substrates of associative or instrumental learning. Rather, differences in factors in the affective domain (state and/or trait anxiety) that influence performance, rather than learning, per se, appear to have been selected genetically.

Animals↗
PubMed2000

Improved conditioned avoidance learning by oxytocin administration in high-emotional male Sprague-Dawley rats.

OBJECTIVE: To examine anti-stress-like properties of oxytocin as a means to improve conditioned avoidance learning in a low-performing, high-emotional, stock of Sprague-Dawley male rats. METHODS: Adult male rats of two stocks of the Sprague-Dawley strain, designated Stock A and Stock B, were treated daily with oxytocin (1 mg kg(-1) s. c.) for 5 days preceding four daily conditioned avoidance acquisition sessions (approximately 20 trials per 15 min session). The Stock B animals were previously characterized as high-emotional based on [1] elevated plasma corticosterone, and lowered plasma oxytocin, levels and [2] decreased reaction time and an increased startle amplitude to an acoustic stimulation. Finally, [3] these animals were unable to acquire a conditioned avoidance response within 5 days of training. RESULTS: The Stock A animals rapidly and statistically significantly acquired the avoidance behaviour within 4 days of daily training, whereas Stock B animals did not improve over this time period. The avoidance performance of Stock B animals was markedly and statistically significantly improved by the oxytocin pre-treatment, whereas the performance of Stock A animals was not affected by the same oxytocin treatment. CONCLUSIONS: Pre-treatment with oxytocin markedly improved avoidance learning in the Stock B high-emotional animals. It is suggested that the improvement is due to previously demonstrated anti-stress-like properties of oxytocin, rendering the animals able to successfully cope with the demands of the conditioned avoidance situation.

Animals↗
PubMed1995

Corrigendum to 'the pentadecapeptide [Ser1]histogranin impairs passive avoidance learning in mice' [Eur. J. Pharmacol. 283 (1995) 251-254].

The peptides, histogranin and [Ser1]histogranin, were recently shown to modulate NMDA receptor function. In the present study, the effects of intracerebroventricular (i.c.v.) administration of [Ser1]histogranin and of the histogranin receptor antagonist, histogranin-(1-10), were examined on step-down type passive avoidance learning in mice. [Ser1]Histogranin (30-60 nmol) impaired retention, after post-training administration, but not when it was administered just prior to the retention assay. Histogranin-(1-10) (60 nmol) facilitated learning during training, without affecting retention. Co-administration of histogranin-(1-10) with [Ser1]histogranin (60 nmol each) led to a significant prevention of [Ser1]histogranin-induced learning impairment. These results indicate that [Ser1]histogranin impairs passive avoidance learning according to the pattern of NMDA receptor antagonists and involving specific histogranin sites.

Animals↗
PubMed2005

Successive negative contrast in one-way avoidance learning in female Roman rats.

The inbred RLA (Roman Low-Avoidance) and RHA (Roman High-avoidance) rat strains have been psychogenetically selected for rapid (RHA) vs. extremely poor acquisition (RLA) of two-way active avoidance. As a consequence of this selective breeding, RLA animals exhibit a higher level of emotionality that can be observed in many anxiety models. The present study was conducted in order to analyze the performance of female RLA, RHA and Wistar rats in a behavioral test of anxiety that involves the reduction of the magnitude of an expected reward: the negative contrast effect that is obtained in one-way avoidance learning by reducing the time spent in the safe compartment. To this aim, three groups of animals (30-1/RLA, 30-1/RHA and 30-1/W) were trained to avoid an electric foot-shock administered in a "danger" compartment, by running from this compartment to a "safe" compartment. We observed an impairment of the avoidance response when time spent in the safe compartment was reduced from 30 to 1 s, when 30-1/RLA and 30-1/W groups were compared with control groups that were trained with a constant safe time (1-1/RLA and 1-1/W, respectively). We also obtained significant differences between 30-1/RLA and 30-1/RHA groups in the postshift phase. These results indicate that RLA rats respond more negatively to the frustration triggered by the reduction in time spent in the safe compartment, suggesting that animal models based on negative contrast effects can be useful tools for studying the genetic basis of anxiety.

Animals↗
PubMed1987

Development of amygdaloid cholinergic mediation of passive avoidance learning in the rat. II. Nicotinic mechanisms.

Young rats 10-30 days of age received bilateral injections of antinicotinic and/or nicotinic agents into the lateral (L), the basolateral (BL), or the cortical (CO) amygdaloid nucleus, and were trained to learn a cool-draft stimulus passive-avoidance task, 17 min later. Mecamylamine produced age- and dose-dependent acquisition deficits; these deficits appeared on day 11, increased similarly after injections into any of the three nuclei until day 16, and decreased thereafter, more rapidly after administration into CO nucleus than after injections into L and BL nuclei. In the latter nucleus, the deficits had nearly disappeared on day 30. Nicotine injected alone induced slight facilitatory effects, significant at 20 days but not reliable at earlier stages. However, nicotine could hinder the antagonistic effects of mecamylamine, when given in combination, as early as the 11th day of age on. The results suggest the existence of nicotinic synaptic elements in the basal lateral part of the rat amygdala; however, these seem to play an important role in passive avoidance learning only during the early stages of ontogenesis.

Acetylcholine↗
PubMed2000

The amygdala modulates memory consolidation of fear-motivated inhibitory avoidance learning but not classical fear conditioning.

Although the lateral and basal nuclei of the amygdala are believed to be essential for the acquisition of Pavlovian fear conditioning, studies using post-training manipulations of the amygdala in the inhibitory avoidance learning paradigm have recently called this view into question. We used the GABA(A) agonist muscimol to functionally inactivate these nuclei immediately after single-trial Pavlovian fear conditioning or single-trial inhibitory avoidance learning. Immediate post-training infusions of muscimol had no effect on Pavlovian conditioning but produced a dose-dependent effect on inhibitory avoidance. However, pre-training infusions dose-dependently disrupted Pavlovian conditioning. These findings indicate that the amygdala plays an essential role in the acquisition of Pavlovian fear conditioning and contributes to the modulation of memory consolidation of inhibitory avoidance but not of Pavlovian fear conditioning.

Acoustic Stimulation↗
PubMed1995

Differential effect of buspirone and diazepam on negative contrast in one-way avoidance learning.

The main aim of the present work was to investigate the effect of buspirone, a 5-HT1A receptor agonist, on successive negative contrast in one-way avoidance learning. Successive negative contrast was induced by shifting rats from a large reward (30 s spent in the safe compartment) to a small reward (1 s). Acute administration of buspirone (0.25, 0.5, 0.75 and 1.0 mg/kg i.p.) did not attenuate the contrast effect, as opposed to that observed for diazepam (1 mg/kg i.p.). The highest dose of buspirone used, however, did interfere with the learning of the avoidance response itself. Chronic buspirone (20 days, 0.5 and 0.75 mg/kg i.p.) did not have any effect on successive negative contrast either. Overall, these results could suggest that the 5-HT1A receptor is not involved in the negative contrast effect studied, quite different to that observed for the gamma-aminobutyric acid (GABA) system. The findings are compared to results obtained with animal models selectively sensitive to some anxiolytic drugs, as are the so-called 'conflict models'.

Animals↗
PubMed1992

Comparative effects of carbamazepine, phenytoin, diazepam and clonazepam on inhibitory avoidance learning in mice.

Four antiepileptic drugs were investigated in an inhibitory avoidance task in mice. Following IP administration 30 min prior to training, carbamazepine (32 mg/kg), phenytoin (30-60 mg/kg), diazepam (2-8 mg/kg) and clonazepam (0.125-0.5 mg/kg) impaired retention. When administered 30 min prior to the retention test none of the drugs under investigation affected retention. The drugs did not affect latencies in the hot plate test. This indicates that in the case of pretraining drug administration effects on retention cannot attributed to elevated pain thresholds. Carbamazepine and phenytoin impaired avoidance learning at doses above those which prevent electroshock induced tonic hindlimb convulsions. Diazepam and clonazepam were effective at lower than anticonvulsant doses. The results of the study are relevant to the evaluation of CNS side effects of anti-epileptic drugs in mice.

Animals↗