Antibodies to GM1 ganglioside inhibit a learned avoidance response.
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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↗
[Effects of chlordiazepoxide on passive avoidance learning in Wistar-Imamichi and F344/Du strain rats].
The present study was designed to investigate the effects of chlordiazepoxide (CDP; 5 and 10 mg/kg, ip) on one-trial step-through passive avoidance learning in Wistar-Imamichi (W-I) and F344/Du (F) strain rats. Step-through latency and the time spent in safety-box were significantly longer in W-I than F rats. The number of animals that attained the 300-s criterion was also larger in W-I than F rats. Therefore, it was concluded that W-I rats showed superior performance in the passive avoidance task as compared to F rats. Taken together, these and the previous results (Iwasaki et al, 1984) that F rats acquired the active avoidance learning more easily than W-I rats, the differences of performance in the two strains would reflect differences of strain-specific response patterns in aversive situations, but not of learning ability. Further, CDP produced a dose-dependent state-dependency in W-I but not in F rats. These strain differences in the effect of CDP were considered to derive from differences in sensitivity to the drug, rather than in the baseline performance level, because comparable strain differences in drug effect were reported in active avoidance learning.
Animals↗
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↗
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↗
Avoidance learning, Pavlovian conditioning, and the development of phobias.
This paper examines the role of Pavlovian conditioning in the acquisition, maintenance and elimination of human phobias. Because many conceptualizations of human fears and phobias are based on data from studies of avoidance learning in animals, we first review theories of avoidance. Our conclusion is that none of the extant theories provides an adequate account of avoidance learning, and we propose a model of avoidance that involves Pavlovian, but not instrumental learning. We then analyse critically arguments that Pavlovian conditioning plays only a small role in the aetiology of fears. Finally, the paper examines the implications of a conditioning model of avoidance for the study of human fears and phobias.
Animals↗
Reward dominance and passive avoidance learning in adolescent psychopaths.
This study tests predictions that adolescent psychopaths are hyperresponsive to rewards (Quay, 1988) and deficient in passive avoidance learning (Newman & Kosson, 1986). Forty male adolescent juvenile offenders were divided into psychopaths and nonpsychopaths using cluster analysis. Subjects were administered a passive avoidance learning task which required learning when to respond to cards associated with either reward or punishment. Results showed a greater responsivity to reward in psychopaths, with no group differences in passive avoidance errors. Results lend support to the view that psychopaths tend to focus on the prospect of reward under conditions of mixed incentives and, when sufficiently motivated, are capable of improved performance. Together with findings of recent psychophysiological studies, these results suggest that adolescent psychopaths may have latent abilities which could have treatment implications.
Adolescent↗
Enhancement of passive avoidance learning through small doses of intra-amygdaloid physostigmine in the young rat. Its relation to the development of acetylcholinesterase.
Passive avoidance learning was studied in young rats 7-20 days old, in control conditions and after bilateral injections of physostigmine into the lateral amygdaloid nucleus. Acquisition in controls was possible from postnatal Day 8 on, progressed markedly after Day 11, and nearly reached maturity by Day 20. Physostigmine differentially altered acquisition depending on the dose: facilitation with low doses, no effect with moderate doses, and impairment with high doses. Enhanced learning through small doses of physostigmine was observed at all ages from Day 8 on, and was greater with 0.2 microgram than with 0.1 microgram. Maturation of the cholinergic innervation of the amygdaloid region was also studied between Days 9-20 using acetylcholine-esterase histochemistry. The results suggest that passive avoidance learning is dependent on amygdaloid cholinergic mechanisms early in life. In addition, very immature cholinergic systems, which are known to be uninfluenced by anticholinergic agents, react to anticholinesterases.
Acetylcholinesterase↗
Place avoidance learning and stress-induced analgesia in the attacked mouse: role of endogenous opioids.
In this study, mechanisms of pain inhibition (tail-flick test) and memory (place avoidance paradigm) were investigated in attacked, DBA/2 and C57BL/6, mice. During training, exposure of test animals to 10 or 30 bites by an aggressive, isolated ICR mouse situated in the dark half of a bright/dark conditioning box induced a significantly higher social conflict analgesia in DBA than in C57 mice. Naltrexone (0.5 and 2.0 mg/kg) reduced this response in DBA mice that received 30, but not 10, bites and was ineffective in C57 mice. This points to different, opioid versus naltrexone-insensitive nonopioid, analgesic mechanisms. During place choice testing in the same box 24 h later, DBA mice that had received 30, but not 10, bites showed a significant, naltrexone-reversible, avoidance of the attack place. No place avoidance learning was observed in C57 mice. The data provided unequivocal evidence that place avoidance learning was a result of associative conditioning, in that neither pairing nor social conflict per se significantly changed the preference for the dark side seen in experimentally naive DBA mice. Antagonism of place avoidance conditioning was observed regardless of whether testing was carried out in the drugged or undrugged state, excluding possible state-dependent effects as an explanation for the naltrexone-induced impairment. Individual correlational analysis in saline-injected, attacked DBA mice revealed a negative relationship between the analgesic state immediately after training and the avoidance of attack place during testing. In summary, the results suggest strain-dependent analgesic and learning mechanisms and indicate that endogenous opioids released in attacked DBA mice support pain inhibition and modulate the memorization of attack place by their analgesic effects, as well as by mechanisms independent of pain inhibitory systems.
Animals↗
One trial passive avoidance learning in neonatally hormone treated rats. Its relation with activity.
The performance in one trial passive avoidance learning and the degree of activity were determined in adulthood, from neonatal hormone treated and intact rats. Activity was measured in the same environmental conditions in which the learning test takes place, i.e., shuttle box unequally illuminated. The treated groups were androgenized females and castrated males. Intact groups were composed by normal males and females. Intact females showed more activity than intact males. Castrated males and androgenized females displayed a degree of activity similar to the normal females. This score was negatively correlated with the total time that each animal remained in the dark compartment of the box. In this respect the normal males showed greater dark preference than the other three groups, which had no differences among them. Similar results to that of dark preference were obtained in performance on one trial passive avoidance learning, that is, androgenization in females did not produce a significant effect in this test and castration in males decreased their performance. A linear correlation between activity and passive avoidance score could be established.
Animals↗
[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↗
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↗
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↗
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↗
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↗
The effect of lithium chloride on one-trial passive avoidance learning in rats.
1 Expression of a one-trial passive avoidance learning response in rats was examined following injections of lithium chloride or sodium chloride before and after initial training and before the first day of testing. Five tests were given at daily intervals, 24 h after training being the time of the first test. 2. Lithium given before the first day of testing impaired response expression on the first and all subsequent days of testing; the rate of extinction was unaffected. 3. Given both before and immediately after initial training, lithium impaired response expression on the first day of testing but slowed down the subsequent rate of extinction, leading eventually to improved performance on the fifth day, as compared with placebo-treated control subjects. 4. The results are interpreted in the light of the hypothesis that lithium impaired the central processing of sensory information.
Animals↗
Behavioral activity and active avoidance learning and retention in rats neonatally exposed to painful stimuli.
Twice daily for the first 15 days after birth, rats from the same litters were either placed for 5 sec on a hot plate (55 degrees C) (treated group), or on a plate maintained at body temperature (38 degrees C) (manipulated group). Controls were left undisturbed. When 90 days old, they were studied for pain threshold, open-field behavior, and two-way active avoidance learning and retention. Weight gain, pain threshold, open-field behavior, and active avoidance retention were not significantly different in the three groups. On the other hand, the rate of two-way active avoidance learning was significantly greater in treated rats. These results suggest that repeated neonatal exposure to painful stimuli, in rats raised under otherwise normal conditions, improves later active avoidance performance. The most likely mechanisms are discussed.
Acoustic Stimulation↗
2-Amino-4-phosphonobutyric acid selectively blocks two-way avoidance learning in the mouse.
There seems to be ample evidence supporting the view that glutamate plays a significant role in the mammalian brain as a neurotransmitter. It is considered to be a likely transmitter candidate in one or more hippocampal pathways. Recently it has been visualized in excitatory, possibly glutamatergic, neurons in the hippocampus. Glutamate has been proposed to mediate memory formation. We wanted to see if blocking glutamate action by a specific glutamate antagonist could result in reduction of learning ability. 2-Amino-4-phosphonobutyric acid (APB) is an analogue of glutamic acid and has been used as a glutamate antagonist in electrophysiological studies on invertebrate neuromuscular junction, retina and hippocampus. We tested the influence of APB on the acquisition of two way avoidance learning in the shuttle box and on learning in the water maze. Our results show that intraperitoneal injection of APB led to a reduction in avoidance learning, whereas learning in the water maze was unaffected.
Aminobutyrates↗