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PubMed1990

[The development of theories of avoidance learning and its application to behavioral pharmacology].

How the development of theories changed the definition of avoidance behavior was discussed. Three major theories of avoidance learning; the two-process theory, the species-specific defense reactions hypothesis, and the cognitive expectancy theory were reviewed. Very few innovations were brought to the experimental apparatuses and procedures by which these theories were tested. The paradigms have been applied without any theoretical considerations. Therefore, I claim here that the modification or renewal of experimental paradigms will be needed to make suitable animal models for psychopharmacology.

Animals↗
PubMed1994

Transient benzodiazepine-GABAA receptor increase after a passive avoidance learning in synaptosomal membranes from chick forebrain.

One-day-old chicks were exposed to a one-time passive avoidance learning task. After chicks peak a bead dipped in a bitter-tasting liquid, they learn to stop pecking the bead. Radioligand binding analysis of [3H]flunitrazepam was performed on crude synaptosomal membranes from forebrains, at 10, 30, and 60 min post-training. Water-trained chicks (control) pecked a bead dipped in water, and they did not learn to stop pecking the bead. The water control was complemented with a methyl anthranilate fed control chick to demonstrate that taste per se does not affect the [3H]flunitrazepam binding. At 30 min in relation to 10 min post-training, the Bmax increased 31% in water-trained chicks and 56% in taste-trained chicks, with Bmax of the taste-trained chicks reaching a value 22% higher than that in water-trained chicks. The difference, attributable to the learning, disappeared at 60 min post-training, and at all times the affinity remained unchanged. The Bmax increase in water-trained chicks might be attributable to psychological stress accompanying the task and the Bmax increase in taste-trained chicks attributable to the learning in addition to the stress accompanying the task. The results suggest that the receptor increase associated with learning is involved in early stages of memory formation.

Animals↗
PubMed1991

Effects of cingulate cortical lesions on avoidance learning and training-induced unit activity in rabbits.

This study extends an ongoing analysis of the neural mediation of discriminative avoidance learning in rabbits. Electrolytic lesions encompassing anterior and posterior cingulate cortex (area 24 and 29) or ibotenic acid lesions in area 24 only were made prior to avoidance conditioning wherein rabbits learned to step in response to a tone conditional stimulus (CS+) in order to avoid a brief, response-terminated 1.5 mA. foot-shock unconditional stimulus (US). The US was presented 5 s after CS+ onset, in the absence of a prior stepping response. The rabbits also learned to ignore a different tone (CS-) not followed by the US. Multi-unit activity of the caudate and medial dorsal (MD) thalamic nuclei, projection targets of the cingulate cortex, was recorded during learning in all rabbits. Activity was also recorded in area 29 in the rabbits with area 24 lesions. Learning in rabbits with combined lesions was severely impaired and it was moderately retarded after lesions in area 24. MD thalamic and caudate training-induced neuronal discharge increments elicited by the CS+ were enhanced in rabbits with lesions, suggesting a suppressive influence of cingulate cortical projections on this activity. Early-, but not late-developing training-induced unit activity in area 29c/d was absent in rabbits with area 24 lesions, indicating that area 24 is a source of early-developing area 29 plasticity. These results are consistent with hypotheses of a theoretical working model, stating that: a) learning depends on the integrity of two functional systems, a mnemonic recency system comprised by circuitry involving area 24 and the MD nucleus and a mnemonic primacy system comprised by circuitry involving area 29 and the anterior thalamic nuclei; b) corticothalamic information flow in these systems suppresses thalamic CS elicited activity in trained rabbits; c) corticostriatal information flow is involved in avoidance response initiation. An absence of rhythmic theta-like neuronal bursts in area 29b in rabbits with area 24 lesions is attributable to passing fiber damage.

Animals↗
PubMed1990

Effects of concurrent manipulations of nicotinic and muscarinic receptors on spatial and passive avoidance learning.

The present study investigates the effects of concurrent manipulations of nicotinic and muscarinic cholinergic receptors on spatial and passive avoidance learning/retention in rats. Daily pretraining test injections of combinations of the subthreshold doses of muscarinic (scopolamine 0.3 mg/kg) and nicotinic (mecamylamine 2.5 mg/kg or 10 mg/kg) antagonists impaired acquisition of the water-maze task (WM). Drug-induced deficits were also observed during the retention trial: the groups injected with scopolamine 0.3 mg/kg, mecamylamine 10 mg/kg and scopolamine 0.3 mg/kg in combination with mecamylamine 2.5 mg/kg showed reduced spatial bias compared with controls. Single preretention test injections of the combination of subthreshold doses of mecamylamine (10 mg/kg) and scopolamine (0.8 mg/kg) impaired memory retrieval in WM. Combined pretraining injections of subthreshold doses of scopolamine (1.0 mg/kg) and mecamylamine (10 mg/kg) induced a severe passive avoidance impairment comparable to 2.0 mg/kg of scopolamine. However, preretention test injections did not impair passive avoidance retention. Either single or combined injections of hexamethonium (5.0 mg/kg, SC) and methylscopolamine (1.0 mg/kg) did not impair either passive avoidance or water-maze performance. The present results suggest that 1) nicotinic and muscarinic systems jointly modulate performance in spatial and avoidance learning tasks and 2) cholinergic antagonists affect acquisition functions more effectively than retention ability. These findings may be relevant to the clinical disorders, like Alzheimer's disease, which are associated with a loss of both cholinergic neurons and nicotinic receptors.

Animals↗
PubMed1982

[The effects of hippocampal lesions on two types of avoidance learning in rats: effects on learning to be active or to be inactive].

Two experiments were conducted to study the effects of hippocampal lesions upon various behaviors of rats in both shock and shock-free situations. The main emphasis, however, was placed on the study of the effects of the lesion upon avoidance learning to be active and inactive. In Experiment I, partially hippocampectomized rats, as compared with the control rats, showed better performance in the avoidance task to be active, but groups did not differ in the avoidance task to be inactive. Having assumed that the latter result was due to the insensitivity of the stabilimeter device used to detect rat's movements, they were detected visually by an observer under a blind condition in Experiment II. Hippocampectomized rats were shown to be poorer than control rats in learning to avoid by being immobile. The results were discussed with reference to Issacson (1974) and Blanchard, Blanchard, Lee, and Fukunaga (1977). The results obtained in shock free situations did not differ significantly among groups. But there was some evidence showing the mean durations of freezing and immobility to be less per episode in hippocampectomized than control rats.

Animals↗
PubMed1979

Effect of p-chlorophenylalanine on avoidance learning of two differentially housed mouse strains.

The effect of p-chlorophenylalanine (PCPA) has been studied on the acquisition of avoidance learning and on brain concentrations of 5-hydroxytryptamine, 5-hydroxyindoleacetic acid and tryptophan of differentially housed male mice of Albino Swiss and DBA strains. The results obtained do not support the hypothesis that learning ability varies inversely with the concentration of brain 5-hydroxytryptamine. PCPA can appear as influencing learning ability of different strains of mice differentially housed, depending more on the emotional baseline of the animals than on brain 5-hydroxytryptamine modification.

5-Hydroxytryptophan↗
PubMed1989

Systemic injection of pirenzepine induces a deficit in passive avoidance learning in rats.

When injected IP, the M1 muscarinic receptor antagonist pirenzepine dose-dependently induced a deficit in passive avoidance learning in rats. This activity was optimal at 75 mg/kg injected 1 h before the acquisition session. The deficit induced by pirenzepine was antagonized by oxotremorine (0.03-0.3 mg/kg SC) and physostigmine (0.1 mg/kg SC), but not neostigmine. By comparison, under the same experimental conditions, physostigmine and oxotremorine also antagonized the deficit induced by an equipotent dose of scopolamine (0.5 mg/kg IP), although the activity of physostigmine appeared stronger against scopolamine than against pirenzepine. These results suggest that pirenzepine could produce a centrally-mediated behavioural disruption when injected systemically.

Animals↗
PubMed1977

Deficits in passive-avoidance learning following atropine in the developing rat.

The maturation of cholinergic inhibitory mechanisms that may be involved in passive-avoidance learning was studied in rats 14, 17, 21, 25, 28, and 34 days of age. Acquisition and extinction of the conditioned response were examined under saline and atropine sulfate (5 mg/kg). Learning was also tested following scopolamine hydrobromide injections (1, 4, 8 mg/kg) in rats 17 days of age and following alpha-methylatropine (5 mg/kg) in 17- and 34-day-old groups. In normal animals the rate of acquisition increased during ontogenesis, with a significant improvement between postnatal days 17 and 21, whereas the rate of extinction did not vary with age. Acquisition was impaired by atropine sulfate at all ages and even totally prevented in younger groups (14 and 17 days of age). It was also completely disrupted by scopolamine in 17-day-old rats. Extinction following acquisition under atropine was more rapid than after normal acquisition. Methyl-atropine was without effect. These results support the hypothesis of central cholinergic mechanisms involved in response suppression, already functioning in the rat 14 days of age and maturing mainly between the 17th and the 21st postnatal days.

Age Factors↗
PubMed1975

Methylphenidate effects on avoidance learning at two ages in the rat.

The major purpose of this investigation was to assess the effects of methylphenidate on avoidance learning at two ages. The subjects were 96 naive albino rats, equally divided between the sexes. One-half received daily drug administrations beginning at 47 days of age; one-half began at 87 days of age. Both groups were divided into three drug dosage levels (0.5, 1.5 and 4.5 mg/kg) and a distilled water control group. Methylphenidate was administered s.c. for a total of 18 days. Following 3 days of drug administrations only, 10 daily trials on avoidance conditioning were administered approximately 10 min after drugging to a total of 150 trials. The major findings indicated that: (1) no significant difference in avoidance response acquisition was obtained in the comparison between drug and control groups, (2) a dose effect was obtained in that the M4.5 group made siginificantly more correct responses than the M1.5 group, and (3) animals drugged beginning at 87 days made significantly more correct responses than those drugged beginning at 47 days.

Aging↗
PubMed1989

Effects of some beta-adrenoceptor blockers on avoidance learning in rats.

In experiments on male Wistar rats, we studied the effects of some beta-adrenoceptor blockers: nonselective-propranolol, pindolol and 3b (a new aminotetraline derivative); and cardioselective (beta 1)-acebutolol and talinolol, on avoidance learning. The nonselective beta-adrenoceptor blockers failed to deteriorate and in some cases even facilitated learning, estimated by the number of avoidance responses and their latencies, while the cardioselective blockers significantly impaired learning process. A significant learning-impairing effect was shown by the beta 2-adrenoceptor agonist salbutamol. Similar was the effect of the mixed alpha- and beta-adrenoceptor blocker labetalol. The results are interpreted in connection with the functional role of beta 1- and beta 2- adrenoceptors in the CNS and with the importance of their balance for learning process.

Adrenergic alpha-Antagonists↗
PubMed1980

Active and passive avoidance learning in controls and schizophrenic patients on racemic propranolol and neuroleptics.

Normal controls and schizophrenic patients on propranolol as sole drug or combined with neuroleptics showed superior active and passive avoidance learning to schizophrenic patients who were medicated with conventional neuroleptics only. Active avoidance involved responding quickly, passive avoidance withholding a response to avoid an unpleasant noise and reacting to the appropriate stimulus. This may reflect an improvement brought about by propranolol in the limbic regulation of stimulus and response processes.

Adult↗
PubMed1988

Influence of hippocampal kindling on avoidance learning in cats.

The formation of avoidance response and differentiation was studied in 13 control and 7 kindled cats with developed hippocampal epileptic focus and complex partial or secondary generalized tonic-clonic seizures. Conditioning sessions lasted from 15 to 20 min in a period following afterdischarges and seizures resulting from electrical stimulation of the hippocampal formation. In two out of seven kindled cats the conditioned reflex was established within time limits (9 and 20 days) comparable to the control cats. These two animals had relatively short-lasting afterdischarges (mean values: 17 and 19 s). In cats with longer-lasting afterdischarges and complex partial seizures (mean duration: 32 to 65 s, in different animals) criterion was not reached during parallel kindling-conditioning stage of 10 to 30 days. The level of correct responses was low and variable (0-70 percent), despite typical reactions to the unconditioned stimuli and clear orienting responses to the conditioning stimuli on more advanced stages of training. Four kindled animals entered the stage of secondary generalization of seizures after hippocampal stimulation. Reflex performance after tonic-clonic seizures was practically abolished. The termination of kindling resulted in acquisition of the conditioned reflex in all the animals. The results indicate, that in animals with long-lasting complex partial seizures the learning of the avoidance response is impaired. In contrast to the effects exerted by afterdischarges and complex partial seizures, intensive interictal hippocampal spiking did not seem to have a direct negative influence on, this particular type of learning.

Animals↗
PubMed1983

Phencyclidine and behavior: II. Active avoidance learning and radial arm maze performance.

Rats with injections of 4 or 8 mg/kg of phencyclidine (PCP) are impaired in the acquisition of active avoidance learning and radial arm maze performance. This impairment was not due to a change in detectability of aversive stimuli or the inability to perform the correct response. The primary deficit appears to be the inability of PCP injected animals to encode the appropriate attributes (e.g., environmental context, response selection, and emotion) associated with each task.

Animals↗
PubMedDate not supplied

Substance P enhancement of inhibitory avoidance learning: mediation by the N-terminal sequence.

Experiments were performed to investigate the effects of intraperitoneally administered undecapeptide substance P (SP), its N-terminal fragment SP(1-7) (SPN) and the C-terminal analog [pGlu6]-SP(6-11) (SPC) on inhibitory avoidance learning, using a one-trial up-hill avoidance task. In Experiment 1 rats were injected with either SP (50 micrograms/kg), SPN (3.3, 33, 167, 333 micrograms/kg) or SPC (2.7, 27, 134, 268 micrograms/kg) immediately after the training trial. Controls received the diluent vehicles. When tested 24 hr later, rats injected with 50 micrograms/kg SP (37 nmol/kg) and 167 micrograms/kg SPN (185 nmol/kg) exhibited longer step-up latencies than vehicle-treated controls. None of the other doses of SPN nor of the C-terminal fragment influenced performance. In Experiment 2, 167 micrograms/kg SPN or vehicle was injected posttrial either immediately or 5 hr after the training trial. Retention latencies 24 hr later were longer for rats treated with 167 micrograms/kg SPN immediately after the training trial. Performance of the SPN 5-hr delay group did not differ from that of the vehicle-injected controls, ruling out proactive effects of SPN on recall.

Animals↗
PubMed1986

Serotonin receptor involvement in the avoidance learning deficit caused by p-chloroamphetamine-induced serotonin release.

The receptor involvement in the p-chloramphetamine (PCA, 2.5 mg kg-1) induced impairment of active avoidance acquisition was examined in the male rat. The avoidance deficit was blocked at low doses by serotonergic (5-HT)-receptor blocking agents but not by alpha-adrenergic-, beta-adrenergic-, opiate-, muscarinic- or dopamine D2-receptor antagonists. The potency of the 5-HT antagonists to block the PCA-induced deficit correlated with their affinity in displacing [3H]ketanserin but not [3H]5-HT binding in the frontal cortex. The potencies of the 5-HT antagonists to block the action of PCA could not be related to their action on muscarinic-, histaminergic H1- or dopaminergic D2-receptor binding in vitro. It is concluded that the avoidance learning deficit caused by PCA-induced 5-HT release is related to activation of 5-HT receptors in the frontal cortex having the characteristics of a 5-HT2 receptor.

Adrenergic alpha-Agonists↗
PubMed1976

Effects of anisomycin on brain protein synthesis and passive avoidance learning in newborn chicks.

The effects of anisomycin (ANM) on newborn chicks have been studied with respect to brain protein synthesis, growth, EEG, toxicity, and several passive avoidance learning tasks. It was found that intracerebral ANM (80 nmol) gave a maximum inhibition of brain protein synthesis of 30%, while a combination of subcutaneous (10 mumol; 53 mg/kg) plus intracerebral (80 nmol; 21 mug) ANM inhibited by 91% in the first 2 hr and by 75% in the subsequent 2 hr period. Cycloheximide (CXM) also in combined injections at the same doses as ANM, inhibited by 97% in the 4 hr that followed injection. However, all the CXM-injected chicks were dead by 18 hr, while the lethality of ANM did not differ from that of saline. ANM also did not affect EEG measured at 1, 3, 5, or 24 hr following the subcutaneous plus intracerebral injections, nor did ANM affect body or brain growth curves or brain protein accretion. In the learning experiments, animals were initially trained to peck at water-coated metal spheres (type A learning) or at water imbibed birdseed (types B and C learning) in less than 1 sec, and were exposed to the same lures treated with the aversant methylanthranilate (MeA) one day later on one occasion (types A and B learning) or exposed twice (type C learning) and tested for learning retention one day later. Learning criterion was set as failure to peck at the lure during the first 20 sec of presentation. If ANM was injected 1 hr prior to MeA exposure, large and highly significant memory deficits were found during the retention test, as compared with saline injected controls. No effect of ANM was seen, however, if it was injected one day after learning, indicating that it did not interfere with retrieval mechanisms. ANM also decreased the external manifestations of fear or displeasure that chicks express during retention testing. Such manifestations have a high correlation with pecking suppression (r = 0.88, P less than 0.001).

Amino Acids↗
PubMedDate not supplied

[The long-term effect of acute hypoxic hypoxia on shuttlebox avoidance learning in rats].

Long-term influence was studied of the acute hypoxic hypoxia seance on rats behaviour in situation of elaboration of the conditioned reaction of active avoidance of electric shocks in shuttle chamber. It was found that in 2.5-3 months after the hypoxia seance, the experimental animals significantly differed from the intact controls by dynamics of CR elaboration (rats which had hypoxia were ahead of the control ones) and by distribution of the conditioned reactions latencies (for experimental animals this distribution was shifted to minor values). The character of these behavioural shifts coincided with that observed in the group of rats with local unilateral hippocampus lesion. The obtained results and numerous data presented in literature on the influence of the hippocampus lesion on animals shuttle avoidance learning, allow to conclude that the seance of hypoxic hypoxia leads to the disturbance of the hippocampus function. This conclusion conforms to the data on diffusive death of the hippocampal and neocortical neurones as a result of hypoxia action.

Acute Disease↗