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Escape and avoidance learning in newly hatched domestic chicks.

Under the conditions specified, chicks fail to learn either to escape or to avoid shock on the day of hatching. Chicks trained for the first time on the day after hatching quickly learn to escape but do not learn to avoid shock. Avoidance learning first appears on the third day of life, and from that time the number of chicks learning to avoid increases with age, so that by the fifth day of life the majority are able to do so.

Animals↗

Comparison of the effects of acute and subchronic administration of atipamezole on reaction to novelty and active avoidance learning in rats.

The effects of an alpha2-adrenoceptor antagonist, atipamezole, on exploratory behaviour in a novel environment, spontaneous motor activity and active avoidance learning were studied after acute injection and continuous infusion (0.1 mg/kg h) for 24 h and 6-9 days in rats. The effects of atipamezole on biogenic amines and their main metabolites in brain were studied after an acute injection (0.3 mg/kg s.c.) and continuous infusion (0.1 mg/kg h) for 24 h and 10 days. The level of central alpha2-adrenoceptor antagonism and the drug concentration in blood and in the brain were measured after continuous infusion for 24 h and 10 days. In behavioural tests, atipamezole had no effect on spontaneous motor activity at any of the doses studied. However, after both acute administration and continuous 24-h infusion, atipamezole decreased exploratory behaviour in a staircase test, but no longer after 6 days of continuous infusion. Acute administration of atipamezole impaired performance in active avoidance learning tests causing a learned helplessness-like behaviour. When the training was started after 7 days of continuous infusion, atipamezole significantly improved active avoidance learning. There was a significant increase in the metabolite of noradrenaline (NA), 3-methoxy-4-hydroxyphenylethyleneglycol sulphate (MHPG-SO4), after 24 h but not any longer after 10 days of continuous atipamezole infusion, although the extent of central alpha2-adrenoceptor antagonism was unchanged and the atipamezole concentration present in brain was even elevated at 10 days compared to levels after 24-h infusion. In conclusion, these results reveal that acute and subchronic atipamezole treatments have different and even opposite effects on behaviour in novel, stressful situations. After acute treatment, atipamezole potentiates reaction to novelty and stress, causing a decrease in exploratory activity and impairment in shock avoidance learning. After subchronic treatment, there was no longer any effect on exploratory behaviour and, in fact, there was an improvement in the learning of a mildly stressful active avoidance test. The changes in behaviour occurred in parallel with attenuation in the MHPG-SO4-increasing effect, thus the suppressed behaviour in the present test conditions after acute atipamezole injection is associated with a major increase in central NA release. The results support the role of alpha2-adrenoceptors and noradrenergic system in reactions both to novelty and stress and have possible implications in cognitive functions as well as in depression.

Adrenergic alpha-Agonists↗

Genetic differences in avoidance learning by Rattus norvegicus: escape/avoidance responding, sensitivity to electric shock, discrimination learning, and open-field behavior.

The behaviors of rats selectively bred for either good or poor shuttle box avoidance learning were studied. The results of Experiment 1 indicated that the phenotypic difference in avoidance learning is not associated with differences in speed of escape or avoidance responding. Differences between the lines in frequency of intertrial responses (ITRs), which appear during training but not during pretest, suggest that ITRs in animals of the low-avoidance (SLA) line are more suppressed by electric shock than in animals of the high-avoidance (SHA) line. This result suggests that SLA animals may be more emotionally responsive than SHA animals. Experiment 2 demonstrated that the animals of the two lines do not differ in absolute sensitivity to electric shock, and Experiment 3 showed that the poor performance of the SLA line is not due to an inability to learn. Experiment 3 also provided evidence which suggests that the poor avoidance learning by SLA animals is due to their emotional reactivity. Observations of open-field behavior in Experiment 4 are consistent with this hypothesis. The major consistent correlate of the phenotypic difference in avoidance learning is greater emotionality or emotional reactivity in SLA than in SHA animals.

Animals↗

Species-specific defense reactions and avoidance learning. An evaluative review.

Bolles (1970) proposed a theory of avoidance learning, the species-specific defense reaction (SSDR) hypothesis, which emphasized innate constraints on the response repertoire of rats in aversive situations and minimized the role of reinforcement in avoidance learning. The present paper describes Bolles' (1970, 1971, 1972, 1975, 1978) development of SSDR theory and reviews the empirical tests of its assumptions and predictions. It is concluded that the SSDRs described by Bolles, along with some others, are highly probable in aversive situations but that the response repertoire is not limited to them. Further, there is strong evidence for reinforcement effects in the establishment and maintenance of at least some avoidance responses.

Aggression↗

The effect of sulfur dioxide inhalation on active avoidance learning, antioxidant status and lipid peroxidation during aging.

The effect of SO2 was examined on active avoidance learning, thiobarbituric acid reactive substances (TBARS), and the activities of Cu, Zn superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in young (3 months), middle-age (12 months ), and old (24 months) Swiss male albino rats. Ten ppm SO2 was administered to the animals of SO2 groups in an exposure chamber for 1 h/day x 7 days/week x 6 weeks while control groups were exposed to filtered air in the same condition. The most prominent effect of aging on active performance was also observed in the older group. SO2 exposure significantly decreased the active avoidance learning in the young group, but it had no effect on this parameter in the middle-aged and the older group compared with their corresponding control groups. SO2 exposure resulted in increased levels of Cu, Zn-SOD activity while decreased level of GSH-Px activity in all experimental groups compared with their corresponding control groups. CAT activities were unaltered. TBARS levels of all SO2 exposed groups were significantly increased compared with their respective control groups. In conclusion, results from the present research showed that SO2 exposure resulted in an increase in the lipid peroxidation and caused alterations in antioxidant enzyme activities. Additionally, SO2 exposure impaired cognitive function only in the young rats during the acquisition phase of active avoidance learning.

Administration, Inhalation↗

[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↗

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↗

Action of C-type natriuretic peptide (CNP) on passive avoidance learning in rats: involvement of transmitters.

The action of C-type of natriuretic peptide (CNP) was tested on one-way passive avoidance learning in rats. The involvement of transmitters was investigated by pretreating the animals with different receptor blockers. CNP administered into the lateral brain ventricle caused a dose-dependent facilitation of learning and consolidation of passive avoidance learning, but was ineffective on retrieval. Pretreatment of the animals with atropine, haloperidol or the nitric oxide synthase inhibitor nitro-L-arginine abolished the action of CNP. Phenoxybenzamine, naloxone, bicuculline, propranolol and methysergide were ineffective in modifying the action of CNP on consolidation. The results suggest that CNP is able to improve the learning and consolidation of learning in a passive avoidance paradigm, but is ineffective on retrieval processes. In the action of CNP, dopamine, acetylcholine and nitric oxide could be the mediating transmitters.

Animals↗

Avoidance learning in schizophrenia: a dissociation between the effects of aversive and non-aversive stimuli.

Patients with schizophrenia did not take significantly more trials than normal controls to learn to use a visual warning signal to avoid a non-aversive stimulus on a simple computer-administered avoidance learning task. When the stimulus to be avoided was aversive (i.e., a loud buzzer), however, the schizophrenic group could be divided into two subgroups based upon their performance; almost one half of the schizophrenic group failed to learn how to avoid this task successfully. The other half, like the normal controls and the closed head injury group in our previous studies, benefited from the aversiveness of the stimulus to be avoided, and learned to avoid more quickly than in the non-aversive condition. A post-hoc analysis of the differences between these two subgroups of the patients suggested that the discrepancy in learning was related to the age of onset of illness.

Adult↗

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↗

The action of orexin A on passive avoidance learning. Involvement of transmitters.

The action of orexin A on one-way passive avoidance learning was studied in rats. Orexin A administered into the lateral brain ventricle in conscious rats facilitated learning, the consolidation of learning and also retrieval processes in a dose-dependent manner in a passive avoidance paradigm. The involvement of transmitters was studied by pretreating the animals with receptor antagonists, which had proved to be effective with other neuropeptides in attenuating or blocking the action of orexin A. The following receptor blockers were used: haloperidol, phenoxybenzamine, propranolol, atropine, bicuculline, naloxone and nitro-L-arginine, which can block nitric oxide synthase. In the doses used all of the receptor blockers attenuated, but none of them fully blocked the action of orexin A on the consolidation of passive avoidance learning. The results demonstrate that orexin A is able to facilitate learning, consolidation of learning and also retrieval processes in a passive avoidance paradigm. A number of transmitters could be involved in the action of consolidation, but none of them is absolutely essential.

Adrenergic alpha-Antagonists↗

Involvement of the telencephalon in spaced-trial avoidance learning in the goldfish (Carassius auratus).

Goldfish (Carassius auratus) received escape-avoidance training in a shuttle-response situation at a rate of a single trial per day. Widely spaced training evaluates the ability of a discriminative stimulus to control an avoidance response in the absence of stimulus carry-over effects from prior recent trials. In Experiment 1, master goldfish exhibited significantly faster avoidance learning than yoked controls. The results suggest that the shuttle response was instrumentally acquired. Experiment 2 demonstrated a significant deficit in the acquisition of avoidance behavior following ablation of the telencephalon. The implications of spaced-trial, telencephalon-dependent avoidance learning, as demonstrated in these experiments for the first time, are discussed in the context of comparative research on instrumental learning in goldfish. These results provide further support for the hypothesis that the fish telencephalon contains an emotional system that is critical for fear conditioning.

Animals↗

Moderate doses of ethanol partially reverse avoidance learning deficits in high-alcohol-drinking rats.

We previously reported that ethanol-naive high-alcohol-drinking (HAD1 and HAD2) rats exhibited selective deficits in active avoidance learning, as compared to low-alcohol-drinking (LAD1 and LAD2) rats, in a signaled bar-pressing task [Alcohol. Clin. Exp. Res. 24 (2000) 1778]. In the current study, we used appetitive and aversive learning tasks to assess whether administration of ethanol influences approach and avoidance learning in HAD and LAD rats. Rats were administered 0.0, 0.5, 1.0, or 1.5 g ethanol/kg body weight during appetitive and aversive conditioning sessions. We found that ethanol impaired acquisition of the appetitive conditioned response in a dose-dependent manner in both HAD and LAD rats, with 1.5 g/kg ethanol producing the greatest deficits. Notably, moderate doses of ethanol (0.5 and 1.0 g/kg) partially reversed avoidance learning deficits in HAD rats, but only when appetitive conditioning preceded aversive conditioning. The highest dose (1.5 g/kg EtOH) abolished avoidance responding altogether in HAD rats. Avoidance responding in LAD rats was not affected by any dose of ethanol. These results are consistent with previous studies suggesting that alcohol preference may be associated with increased fear or anxiety, but the conditions under which ethanol produces a reduction of fear and anxiety in HAD rats appear to be relatively complex.

Alcohol Drinking↗

Effects of pituitary adenylate cyclase polypeptide (PACAP) on extinction of active avoidance learning in rats: involvement of neurotransmitters.

The effects of PACAP-38 on the extinction of active avoidance learning were studied in rats. The action of transmitter mediation was followed by pretreating the animals with appropriate receptor antagonists. PACAP-38 administered into the lateral brain ventricle caused a transitory facilitation of the extinction of a learned active avoidance response at 3 and 6 h following extinction, which had returned to or even above the control level at the 24-h testing. PACAP 6-38, which is an antagonist of PACAP-38, and an antibody against PACAP-38, prevented this action. When the animals were retested during a further 10 days, the control animals demonstrated response extinction on day 7, while the PACAP-38-treated animals still showed a high proportion (70%) of positive responses. The following receptor blockers diminished the action of PACAP-38 on the facilitation of extinction: propranolol, haloperidol, naloxone, bicuculline and nitro-L-arginine, the latter by blocking nitric oxide formation. Phenoxybenzamine and atropine were ineffective. The data reveal that the transitory action of PACAP-38 within 24 h on the facilitation of extinction is mediated by beta-adrenergic, dopaminergic, GABA-ergic and opiate receptors and nitric oxide. This transitory facilitated extinction is caused partly by depressed locomotion and presumably also an increased body temperature. Following a transitory facilitation of extinction from 24 h on, PACAP-38 demonstrated a greatly delayed extinction, which lasted for more than 7 days, while the control animals displayed complete extinction. The data suggest that PACAP-38 facilitates memory retrieval processes in the extinction of the active avoidance reflex.

Adrenergic beta-Antagonists↗

Long-term potentiation in the rat hippocampal CA1 region is inhibited selectively at the acquisition stage of discriminatory avoidance learning.

Long-term potentiation (LTP) of hippocampal synaptic efficacy has been regarded as a synaptic model of learning and memory. We examined whether the induction of LTP in the hippocampal regions was altered with the advance of discriminatory avoidance learning. Evoked potentials in the CA1 region or dentate gyrus were recorded before and after tetanic stimulation in anesthetized rats which had been given training sessions 24 h before. LTP of the amplitude of population spikes and the slope of excitatory postsynaptic potentials recorded in the CA1 region was smaller in rats at a learning stage 24 h after the avoidance rate had first been significantly increased than in naive rats. The magnitude of LTP was not altered in rats which had been exposed to the first training session or in those which had received overtraining. The inhibition of LTP in the CA1 was neither due to stress accompanied with training nor liberation from the stress by learning avoidance response. In contrast, LTP induced in the dentate gyrus was rather enhanced at the learning stage when LTP in the CA1 was inhibited. The results suggest that the acquisition of discriminatory avoidance learning selectively inhibits LTP in the hippocampal CA1 region.

Animals↗

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↗

Glycine(B) receptor antagonists and partial agonists prevent memory deficits in inhibitory avoidance learning.

Activation of N-methyl-d-aspartate (NMDA) receptors has been hypothesized to mediate certain forms of learning and memory. This hypothesis is based on the ability of competitive and uncompetitive NMDA receptor antagonists to disrupt learning. We investigated the effects of glycine site antagonists and partial agonists on deficits of acquisition (learning) and consolidation (memory) in a single trial inhibitory avoidance learning paradigm. Posttraining administration of either hypoxia (exposure to 7% oxygen) or the convulsant drug pentylenetetrazole (PTZ) (45 mg/kg) to mice impaired consolidation without producing neuronal cell death. Pretreatment with the competitive glycine antagonist 7-chlorokynurenic acid (7KYN) and the glycine partial agonists 1-aminocyclopropanecarboxylic acid (ACPC) and (+)HA-966 prevented memory deficits induced by hypoxia and PTZ, but did not affect scopolamine-induced learning impairment. In addition, ACPC prevented consolidation deficits evoked by a nonexcitotoxic concentration of l-trans-pyrrolidine-2, 4-dicarboxylate, a competitive inhibitor of glutamate transport that increases extracellular levels of glutamate. Moreover, (+)HA-966, 7KYN, and ACPC facilitated both acquisition and consolidation of inhibitory avoidance training, an effect that was dose-dependent and reversed by glycine. These results indicate that memory deficits induced by both hypoxia and PTZ involve NMDA receptor activation. Furthermore, the present findings demonstrate that glycine site antagonists and partial agonists prevent memory deficits of inhibitory avoidance learning by affecting consolidation, but not acquisition processes.

Animals↗