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At least 19 recordsLinked to original sources
PubMed1991

Basolateral amygdaloid multi-unit neuronal correlates of discriminative avoidance learning in rabbits.

Basolateral (BL) amygdaloid multi-unit activity was recorded as male albino rabbits learned to avoid a foot-shock unconditioned stimulus (US) by stepping in an activity wheel to an acoustic (pure tone) warning stimulus (CS+). A second tone (CS-) of different auditory frequency than the CS+ was presented in an irregular order on half of the conditioning trials but was never followed by the US. BL amygdaloid neurons developed, in the first session of conditioning, enhanced CS-elicited discharges relative to discharges recorded during pretraining with tones and noncontingent US presentations (excitatory plasticity), and greater discharges to the CS+ than to the CS- (discriminative plasticity). The discriminative plasticity attained maximal magnitude as the rabbits reached the asymptote of behavioral discrimination, and persisted during post-asymptotic training. Peak excitatory plasticity occurred in the session of the first significant behavioral discrimination and declined during the asymptotic and post-asymptotic stages of training. Similar patterns of excitatory and discriminative plasticity in structures directly interconnected with the BL nucleus (anterior cingulate cortex; medial dorsal thalamic nucleus) and effects of lesions suggest that the neurons in these areas participate in a circuit involved in mediation of avoidance learning.

Amygdala↗
PubMed1976

Does the rat with hereditary hypothalamic diabetes insipidus have impaired avoidance learning and/or performance?

Avoidance learning and extinction of rats with hereditary hypothalamic diabetes insipidus (Brattleboro strain) were studied in 2 experiments that differed only in shock intensity. In both experiments rats homozygous for diabetes insipidus were more deficient in both escape and avoidance responding than were their heterozygous or normal controls. Although the hterozygous animals showed improved escape performance at the higher shock intensity, their avoidance behavior was not improved. The superiority of normal and heterozygous animals in extinction performance, relative to the homozygous animals, was eliminated or reversed when the differences in terminal acquisition performance were taken into account by analyses of covariance. Deficiency of ADH, therefore, may not result in faster extinction of avoidance behavior.

Animals↗
PubMed2026

A systematic review of human avoidance learning: Cognition, computation, and methods.

Avoidance behaviour is fundamental for survival but can become maladaptive in clinical conditions. A large body of literature has accumulated on the dynamics of human avoidance learning. However, current theories and overviews do not provide an exhaustive account of this evidence. In this systematic review, we identify N = 116 studies on human avoidance learning. We analyse these studies with the goal of distilling robust empirical phenomena as a basis for theory-building, and examine their diagnostic value in differentiating between competing theories. We find that the evidence is difficult to reconcile with foundational two-factor and classical safety-signal accounts, and most strongly supports expectancy- and inference-based views, in which avoidance responses are selected with respect to represented consequences. At the same time, no current framework provides a complete account of the evidence: several findings point to an additional role for operant valuation, Pavlovian influences, and contextual or latent-state control over the expression of avoidance. Methodologically, we observe that the problem setting in the most common experimental paradigms is radically simpler than real-world avoidance and therefore unlikely to expose the limits of inferential or reflective mechanisms. Consequently, we argue that paradigms with greater computational demands and more realistic action affordances are required to identify the mechanisms underlying avoidance learning. Collectively, these insights provide a foundation for theoretical refinement, computational modelling, and methodological innovation, with implications for advancing interventions targeting maladaptive avoidance.

Humans↗
PubMed1976

Sensory responsiveness and avoidance learning in rats.

Analysis of sensory responsiveness and avoidance learning was carried out in three experiments using five rat strains. There were significant differences among the strains in response to electric footshock. Also the strain-specific shock intensity as unconditioned stimulus (US) elicited significantly higher rates of avoidance learning as compared with the rates of avoidance learning under an equal but average level of shock intensity as US. In general, discrete auditory and visual sensory modes as conditioned stimuli (CS) produced almost the same rate of avoidance learning. The proportion of variation in avoidance learning attributable to strains was significant under all six experimental conditions except no-discrete CS and strain-specific US condition.

Acoustic Stimulation↗
PubMed1976

Chemical sympathectomy and two-way escape and avoidance learning in the rat.

Six experiments are reported on the effects of 2,4,5-trihydroxyphenylethyl-amine (6-hydroxydopamine) on two-way escape and avoidance learning. Rats were tested on either escape or avoidance learning at 80 days of age after chemical sympathectomy at birth or 40 or 80 days of age. Neonatal and chronic sympathectomy (at 40 days), but not acute sympathectomy (at 80 days), resulted in depressed escape learning. Avoidance learning was affected by neonatal sympathectomy and partially by acute sympathectomy. The results have implications for the role of the autonomic nervous system in escape-avoidance learning.

Age Factors↗
PubMed1988

Opposite effects induced by low and high doses of apomorphine on single-trial passive avoidance learning in mice.

The effects of apomorphine (0.0125-1 mg/kg, SC), a dopamine (DA) agonist, on passive avoidance learning were assessed in mice which received brief and long foot-shocks in a training test. At low doses, apomorphine stimulates DA autoreceptors. With a shock of brief duration, apomorphine at a low dose (0.05 mg/kg), enhanced the avoidance learning when it was administered 20 min before the training test or the retention test. At high doses, apomorphine stimulates postsynaptic DA receptors. With a shock of long duration, apomorphine at a high dose (1 mg/kg), impaired the avoidance learning when it was administered 20 min before the training test or the retention test. However, apomorphine (0.05 and 1 mg/kg) given immediately after the training test did not have any effect on the avoidance behavior with shocks of either brief or long durations. Apomorphine-induced enhancement of passive avoidance learning was antagonized by sulpiride, but not by haloperidol. These results show that apomorphine induced the opposite effects on the passive avoidance learning depending on the dose or on the reinforcement intensity and suggest that the central DA system may play an important role in modulating memory processes.

Animals↗
PubMed1979

Postnatal alpha-methylphenylalanine treatment effects on adult mouse locomotor activity and avoidance learning.

Neonatal mice were injected for five days with a combination of alpha-methylphenylalanine and phenylalanine to determine the influences of excess phenylalanine during development upon the behavior of these mice as adults. Spontaneous activity, bolus production, passive avoidance learning, simple active avoidance learning and complex active avoidance learning were tested in mice treated at two different postnatal periods. The results show that the treatments during development produced adult behavioral alterations compared to controls. The effects were most pronounced in mice treated in the postnatal period immediately after birth. The behavioral effects can be summarized as increased emotionality and generalized, stimulus-induced activity as well as decreased passive avoidance performance and complex active avoidance performance. These behavioral deficits are consistent with those usually reported in various models of human phenylketonuria.

Animals↗
PubMed1985

Forebrain serotonergic involvement in avoidance learning.

The one-way active avoidance deficit caused by the serotonergic (5-HT) releasing compound p-chloroamphetamine (PCA) was examined in rats after degeneration of 5-HT neurons in the forebrain. Injection of 5,7-dihydroxytryptamine (5,7-DHT) into the forebrain in desipramine (20 mg/kg)-pretreated rats resulted in a 65-70% decrease in 5-HT concentrations in the prefrontal cortex and hippocampus without any significant effect on striatal 5-HT. Slight reductions in noradrenaline (NA) (25%) and dopamine (DA) (34%) concentrations were observed in the prefrontal cortex only. The 5,7-DHT lesions markedly attenuated the impaired avoidance performance induced by PCA (2.5 mg/kg), suggesting that the avoidance deficit depends on intact 5-HT terminals in cortex and/or hippocampus. The 5,7-DHT lesion alone caused a slight but significant impairment of acquisition. The results suggest that 5-HT terminal systems in the forebrain play an important role in avoidance learning.

5,7-Dihydroxytryptamine↗
PubMed1990

[Escape-avoidance learning in two strains of inbred mice when two types of response can be alternatively effective].

Three experiments demonstrated that escape-avoidance learning is closely related to the response type dominantly occurred in mice of an inbred strain. Inescapable shock elicited locomotion (L-typed response) in C57BL/6 mice, and rearing or jumping (R-typed response) in C3H/He (Experiment 1). In the shuttle-box situation where both of these responses can be effective to terminate CS tone and electric shock, C57BL established L-typed avoidance mainly, while C3H tended to learn avoidance by R-typed response (Experiment 2). The two strains learned the escape in the shuttle-box by the same types of response as they showed in avoidance learning (Experiment 3). These findings lead us to conclude that different inbred strains of mice innately react to electric shock by their specific types of response. Strain differences in escape-avoidance learning could thus be attributed to the compatibility of the specific response type with requirement of the task situation.

Animals↗
PubMed1988

CER suppression, passive-avoidance learning, and stress-induced suppression of drinking in the Syracuse high- and low-avoidance strains of rats (Rattus norvegicus).

The Syracuse strains of Long-Evans rats were selectively bred for good (SHA) or poor (SLA) avoidance learning in a two-way shuttle box, which resulted in a phenotypic difference that is correlated with behavior patterns indicative of emotional reactivity, SLA animals showing evidence of greater emotional reactivity than SHA animals. The first three experiments examined conditioned suppression of bar pressing and compared paired and unpaired conditioned- and unconditioned-stimulus presentations to evaluate the influence of conditioning versus primary aversive stimulation on baseline responding. SLA animals acquired conditioned suppression faster than SHA animals and also showed greater suppression of baseline responding than SHA animals. In Experiment 4, SLA animals learned a passive-avoidance task faster than SHA animals. In Experiment 5, SLA animals showed greater stress-induced suppression of drinking a weak quinine solution than SHA animals. These data are consistent with the hypothesis that SLA animals are more emotionally reactive than SHA animals.

Animals↗
PubMed1990

Oxiracetam prevents mecamylamine-induced impairment of active, but not passive, avoidance learning in mice.

The nicotinic antagonist mecamylamine (2.5 and 5 mg/kg/IP) depressed both active (shuttle-box) and passive (step-through) avoidance learning in mice of the DBA/2 strain. The nootropic drug oxiracetam (50 and 100 mg/kg/IP) improved acquisition in the multitrial active avoidance test, but had no effect on one-trial passive avoidance learning. When the two drugs were combined, oxiracetam did not counteract mecamylamine-induced impairment of passive avoidance learning, even if it maintained a facilitating action on shuttle-box avoidance acquisition in mice receiving the nicotinic receptor blocker. Prevention of mecamylamine-induced shuttle-box avoidance depression by oxiracetam indicates that central nicotinic mechanisms are probably involved in the improving effects exerted by nootropic drugs on learning.

Animals↗
PubMed1985

Avfail in color avoidance learning by starlings (Sturnus vulgaris) and red-winged blackbirds (Agelaius phoeniceus).

Certain unconditioned stimuli (UCS) in flavor avoidance learning sometimes become ineffective after pairings with relatively stronger UCS. This failure of avoidance learning (avfail) has been demonstrated only with rodents. The present investigations were conducted to determine whether avfail might also occur with avian species, the food selection of which is guided primarily by visual cues. In Experiment 1, starlings were given pairings of methiocarb (a relatively weak UCS) and LiCl (a relatively strong UCS). In Experiment 2, red-winged blackbirds were given pairings of two concentrations of methiocarb (relatively weak and relatively strong UCS, respectively). Pairings were followed by a conditioning trial (UCS gavage in the presence of a color cue) and two-choice tests. Conditioned avoidance was always observed except when methiocarb preceded LiCl and when the low preceded the high methiocarb dose in preconditioning pairings. Experiment 3 demonstrated that UCS habituation could not account for the results of Experiments 1 and 2. The data reflect avfail in the visual modality, and a biological implication of the results is that birds may not learn strong avoidance of aposematic prey containing varied levels of toxicant.

Animals↗
PubMed1988

Does avoidance learning only depend on mossy fiber distribution?

Rats and mice with a poor active avoidance behavior in the shuttle box exhibit a larger extent of the zone innervated by mossy fibers in the infrapyramidal area of the hippocampal sector CA3. The question arose whether only these differences in the amount of inputs from granular cells do correlate with poor avoidance learning, or whether cholinergic septal inputs are likewise related to behavioral performance. Inbred and non-inbred rats with low and high avoidance scores were used. Freezing sections were alternately used for TIMM-staining and for the histochemical visualization of the acetylcholinesterase activity. In comparison with "good avoidance learners" the rats with "poor active avoidance performance" exhibited a larger zone of mossy fibers and a lower activity of acetylcholinesterase in the investigated field. A significant inverse correlation between mossy fiber innervation and cholinergic septal inputs could be established. Our findings suggest that poor avoidance learning does not simply depend on mossy fiber distribution but seems to be dependent rather on the relation between mossy fiber innervation and cholinergic septal inputs.

Acetylcholinesterase↗
PubMed1976

Effect of midbrain raphe lesion on avoidance learning in aggressive mice.

Lesion of the midbrain ventral raphe nucleus greatly improves the avoidance-learning efficiency of normal and isolated-aggressive Albino Swiss mice. Since the lesion of this brain area selectivity lowers the forebrain concentration of 5-hydroxytryptamine (5-HT), implications of the role of brain 5-HT in avoidance-learning acquisition are discussed.

Aggression↗
PubMed1985

Evidence for a role of brain serotonergic neurotransmission in avoidance learning.

This thesis has analyzed the role of brain serotonergic (5-HT) neurotransmission in avoidance learning in the male rat using neurochemical, pharmacological and behavioural approaches. The acute and long-term effects of p-chloroamphetamine (PCA) on one-way and two-way active avoidance (AA) acquisition and retention and passive avoidance (PA) retention and on central monoamine concentrations were examined in the male rat. The effects of PCA were compared with the 5-HT synthesis inhibitor p-chlorophenylalanine (PCPA). To characterize the effects of PCA the following neurotoxins were used: 5,6- and 5,7-dihydroxytryptamine (5,6- and 5,7-DHT) and N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4). The concentrations of biogenic monoamines and their metabolites in discrete brain regions were determined by high pressure liquid chromatography with or without electrochemical detection. The effects on 5-HT receptors in vitro and in vivo were measured by ligand binding studies (using 3H-5-HT and 3H-ketanserin as radioligands) and with behavioural techniques, respectively. Administration of the 5-HT releasing compound PCA prior to training (pre-training) produced a dose- and time-related impairment of one-way AA acquisition and retention and PA retention. A series of studies indicated that the avoidance learning deficits caused by PCA are produced by release of 5-HT, resulting in stimulation of postsynaptic 5-HT receptors. For instance, the avoidance deficit was blocked by pretreatment with the 5-HT uptake inhibitors alaproclate and zimeldine, which inhibit the 5-HT release induced by PCA. The avoidance deficits could not be related to changes (direct or indirect) in NA and DA transmission. Lesion experiments in combination with biochemical analyses provided evidence that the avoidance deficit caused by PCA involves 5-HT terminals of the forebrain, while the descending 5-HT projections seem to play a minor role. The AA acquisition deficit induced by PCA appears to be mediated via stimulation of 5-HT2 receptors, whereas the PA retention is mediated via 5-HT1 receptors. Analysis of the PCA-induced AA deficit indicated that it is mediated by non-associative factors. Thus, the performance of the PCA-treated rats was susceptible to interference from extratask contextual stimuli. Pre-training administration of PCA was found to produce a time-dependent loss in memory retention (PA retention) in animals which had acquired the response. This finding indicates that serotonin also has a role in associative learning processes e.g. in the way information is processed in the rat brain following acquisition.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Effort and stress influence the effect of lesion of the habenula complex in one-way active avoidance learning.

Previous studies which have examined the effects of lesions of the habenula on active avoidance learning have not provided unambiguous support for response deficits. Moreover, interpretation of early studies is confounded by large lesions which damaged adjacent structures. We report the effects of smaller circumscribed lesions of the habenula complex on a simple one-way active avoidance paradigm in three separate experiments in which the required operant was a step or jump onto an elevated platform. In the first study involving avoidance of shock of low intensity (0.5 mA) with an average long intertrial interval of 8 minutes, lesioned animals were not significantly different from sham operated controls. However, in following experiments in which stress levels were increased by raising the shock intensity and reducing the intertrial-interval, or in which the operant was made considerably more demanding by raising the height the animals had to jump to make an avoidance response, there were large lesion induced deficits in avoidance responding. The absence of significant differences between lesioned and sham operated controls in escape latencies suggested no lesion induced impairment of the response to the shock. It is suggested that the data not only support an effect of habenular lesions on active avoidance learning but also are consistent with a previous suggestion that the functional effects of lesion of the habenula on behaviour are effected through changes in dopaminergic function.

Animals↗
PubMed1992

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

In three experiments, successive negative contrast was examined in one-way avoidance learning. Reward magnitude in first (pre-shift) and second (post-shift) phases was manipulated by time spent in the safe compartment. Experiment 1 demonstrated that when time in the danger compartment was held constant, a group shifted from a large reward--30 sec spent in the safe compartment--to a small reward--1 sec--showed poor performance and longer response latency than a group conditioned with the small reward in both phases. Experiment 2 replicated this effect with a less intense shock and also demonstrated that a group shifted from large to small reward performed more poorly than a group exposed to large reward--30 sec--in both phases. Finally, Experiment 3 showed that changes in intertrial interval, defined as total time spent in the safe compartment and the danger compartment before the onset of the warning signal, were not responsible for this contrast effect. These results suggest that time spent in a safe place can act as appetitive incentive during one-way avoidance learning.

Animals↗