Avoidance and escape learning: simultaneous acquisition of different responses.
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Animals↗
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[The characteristics of the participation of the neostriatal cholinergic system in regulating different forms of defensive behavior].
The effects of microinjections of the cholinergic agonist (carbacholine) into the dorsal part of the neostriatum on discrimination processing of sensory signals were studied in chronic experiments in dogs (instrumental defensive reflex connected with maintenance of flexion posture) and in rats (active avoidance learning in T-maze). It was found that an improvement of discrimination process after carbacholine injections was manifested as an increase in the number of correct responses during acquisition of discriminative avoidance reflex in T-maze (rats) and during differentiation of sound signals in instrumental defensive reaction (dogs). The efficacy of this influences was suggested to be depend on the level of animal learning. We did not shown an improvement of the responses in two cases: 1. When before the microinjections the responses on the defensive and on the discriminative signals did not distinguish; 2. Under total differentiation of signals (e. g. under total learning). In both cases the neostriatum seems to be not involved in behavioral reaction what could be accompanied by low neuronal activity during the these signals action.
Acetylcholine↗
Involvement of glutamate receptors, protein kinases, and protein synthesis in memory for visual discrimination in the young chick.
Two-day-old chicks were trained to discriminate between edible chick crumbs and arrays of colored beads glued to the floor of their cage. Normal chicks learned this task within a few minutes and retained it for at least 24 h. The role of several biochemical systems known to be required for other forms of early learning in the chick was explored in this task. Antagonists and inhibitors of these systems were used in the doses known to produce amnesia in a related passive avoidance learning model. Drugs were injected intracerebrally just before training, and retention was tested at various times subsequently. The protein synthesis inhibitor anisomycin (240 nmol/chick) was without effect on retention at 30 min posttraining, but chicks were amnestic at 3 and 24 h. The protein kinases inhibitors melittin (1.2 nmol/chick) and 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine hydrochloride (100 nmol/chick) were without effect on retention at 30 min posttraining but were amnestic by 3 h. While these effects are similar to those found for one-trial passive avoidance training, neither the N-methyl-D-aspartate receptor antagonists (+)-5-methyl-10, 11-dihydro-5H-dibenzo[a, d]cyclohepten-5,10-imine maleate (up to 15 nmol/chick) or DL-2-amino-5-phosphonovalerate (1.3 nmol/chick), both of which are amnestic for passive avoidance, nor the non-NMDA-glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2, 3,-dione (4 nmol/chick) were amnestic for the visual discrimination task. By contrast, the metabotropic glutamate receptor blocker (RS)- alpha-methyl-4-carboxyphenylglycine (300 nmol/chick) injected 5 min pretraining resulted in amnesia at 3 h posttraining. The implications of these findings for the putative "memory consolidation cascade" are discussed.
Animals↗
Extinction and reacquisition of a fear-motivated memory require activity of the Src family of tyrosine kinases in the CA1 region of the hippocampus.
Evidences indicate that extinction represents a NMDA receptor (NMDAr)-dependent learning rather than erasure of previously stored information. Several members of the Src family of tyrosine kinases are activated by stimulation of the NMDAr and are involved in both induction of hippocampal long-term potentiation and consolidation of hippocampal-dependent, NMDAr-sensitive, memories. Here we analyzed the role of the Src family within the CA1 region of the hippocampus in extinction and reacquisition of the memory for step-down, inhibitory avoidance learning task (IA). Rats trained in IA were submitted to 5 daily extinction sessions during which the avoidance response was elicited in the absence of the unconditioned stimulus. Immediately or 180 min after each extinction session animals received intra-CA1 infusions of either 0.1% DMSO, the Src-family inhibitor PP2 or its inactive analog, PP3. PP2 blocked extinction of the IA response which was otherwise evident in DMSO and PP3-treated animals. After being submitted to a new training session the animals reacquired the avoidance response; however, they failed to do so if they received intra-CA1 infusions of PP2 immediately following retraining. Our results indicate that, like the original learning, extinction and reacquisition of the IA response require activity of the Src family in the CA1 region of the hippocampus.
Animals↗
Effects of oral administration of soybean lecithin transphosphatidylated phosphatidylserine on impaired learning of passive avoidance in mice.
Soybean lecithin transphosphatidylated phosphatidylserine (SB-tPS) was investigated for its effect on the impaired learning of a passive avoidance task by mice induced by scopolamine or cycloheximide. SB-tPS (240, 360, 480 mg/kg) administered orally significantly prolonged the step-through latency shortened by scopolamine. SB-tPS (240 mg/kg) administered orally also prolonged the step-through latency shortened by cycloheximide. These results suggest that the effect of SB-tPS on the impaired learning behavior may be related not only to the cholinergic system but also the serotonergic system.
Administration, Oral↗
[Training and extinction of passive avoidance in mice lacking monoamine oxidase A].
The passive avoidance learning and memory trace retention in mice lacking monoamine oxidase A (MAO A) and control C3H strain were analyzed. It is shown that mice of both strains were well the passive avoidance learners. A delay of the memory trace extinction was found in lacking MAO A mice as compared with control C3H strain. Mice with a genetic MAO A knockout showed decreased amounts of transitions, rearings, looking to a dark compartment and appearing from it. These findings seem to reflect more expressed fear reaction to a dangerous compartment and increased anxiety promoting longer retention of memory trace on a high level of retrieval.
Animals↗
A 2-year longitudinal study of swimming navigation in mice devoid of the prion protein: no evidence for neurological anomalies or spatial learning impairments.
Uncontrolled accumulation of a conformationally distorted protein (PrP(Sc)) is supposed to be the pathological process leading to spongiform encephalopathy. Targeted disruptions of the Prn-P gene in the mouse have resulted in animals that did not show anomalies in spatial and avoidance learning and were resistant to experimental infections. However, another Prn-P knockout mouse was reported to show ataxia and Purkinje cell degeneration developing after 70 weeks of age. In this study the initial observations are confirmed on swimming navigation of PrP-null mutant mice using an enlarged sample of 58 mice. A representative subsample of 16 mice was then followed up for their ability of swimming navigation up to an age of two years (104 weeks). Surviving PrP-null mutants (n = 4) and controls (n = 6) did not differ in any measure, nor were there indications of ataxia and Purkinje cell degeneration. It was concluded that the PrP-knockout mice used by Büeler et al. were probably normal with respect to aging processes and that resistance to scrapie is not necessarily paid for by late neuronal degeneration. The reasons for the discrepancy between different knockout experiments require experimental clarification, however.
Animals↗
Inhibition of hippocampal Jun N-terminal kinase enhances short-term memory but blocks long-term memory formation and retrieval of an inhibitory avoidance task.
Learning initiates a series of plastic events the occurrence of which are required for the storage of information related to the training experience. Several lines of evidence indicate that, in the rat hippocampus, different members of the family of mitogen-activated protein kinases (MAPK) play a key role in the onset of such plastic events. Using SP600125, the newly developed inhibitor of the MAPK c-Jun amino-terminal kinase (JNK), we show a direct involvement of this protein kinase in mnemonic processes. The intra-CA1 infusion of SP600125, at a dose that in naïve animals significantly reduced the phosphorylation levels of c-Jun without affecting the activity of ERK1/2 or p38 MAPK, enhanced short-term memory (STM) but blocked long-term memory (LTM) formation and retrieval of an inhibitory avoidance learning task. No action of this drug on locomotor/exploratory activity or general anxiety state could be detected. The significance of these results is discussed in the context of others describing the independence of LTM from STM.
Animals↗
Differential distribution of L-aspartate- and L-glutamate-immunoreactive structures in the arcopallium and medial striatum of the domestic chick (Gallus domesticus).
The role of amino acid neurotransmitters in learning and memory is well established. We investigated the putative role of L-aspartate as a neurotransmitter in the arcopallial-medial striatal pathway, which is known to be involved in passive avoidance learning in domestic chicks. Double immunocytochemistry against L-aspartate and L-glutamate was performed at both light and electron microscopic levels. L-aspartate- and L-glutamate-immunoreactive neurons in the arcopallium and posterior amygdaloid pallium were identified and counted by using fluorescence microscopy and confocal laser scanning microscopy. Most labeled neurons of arcopallium were enriched in glutamate as well as aspartate. However, the arcopallium and posterior amygdaloid pallium differed from a neighboring telencephalic region (nidopallium; formerly neostriatum) by containing a substantial proportion of cells singly labeled for L-aspartate (15%, vs. 5.3% in the nidopallium). Aspartate-labeled neurons constitute approximately 20%, 25%, 42%, and 28% of total in the posterior amygdaloid pallium and the medial, dorsal, and anterior arcopallia, respectively. Immunoelectron microscopy showed that L-aspartate was enriched in terminals of the medial striatum. The labeled terminals had clear and round vesicles and asymmetric junctions; similar to those immunoreactive to L-glutamate. Axon terminals singly labeled for L-aspartate made up 17% of the total. In addition, 7% of neuronal perikarya and 26% of all dendritic profiles appeared to be labeled specifically with L-aspartate but not L-glutamate. The results indicate that L-aspartate may play a specific role (as distinct from that of L-glutamate) in the intrinsic and extrinsic circuits instrumental in avian learning and memory.
Animals↗
Behavioural evaluation of long-term neurotoxic effects of NMDA receptor antagonists.
High doses of NMDA antagonists e.g. (+)MK-801 evoke neurodegeneration in retrosplenial cortex in rodents. To assess functional consequences of such treatment, three paradigms of two-way active avoidance learning (with visual or auditory conditioned stimuli) and additionally a spatial learning paradigm - radial maze - were used. Female rats were treated i.p. with 5 mg/kg of (+)MK-801. Recumbence, severe hypothermia and loss of body weight were observed for 3-7 days. Despite that, there were no statistically significant differences in performance of avoidance reaction between saline and (+)MK-801 treated animals trained 10-40 days after the drug administration. However, in the radial maze test (+)MK-801 impaired reference (but not working) memory in the experiment that started 8 days after the treatment. Similar effect was observed on reversal learning. The clinically used NMDA receptor antagonist memantine at the doses of 20 and 40 mg/kg had also no such long term negative effect on working memory during training (even positive effect was seen at 20 mg/kg) but at 40 mg/kg impaired learning on the first day of reversal. This indicates that (+)MK-801 neurotoxicity in the retrosplenial cortex is connected with subtle alterations in the learning performance that may be seen in some tests only. Moreover, memantine doses greatly exceeding therapeutically relevant range produce minimal functional alteration. An additional experiment revealed that the same dose of memantine results in two fold higher serum levels of the antagonist in female than male rats. Hence, considering that profiling studies are done in male rats, a safety factor of over 16 fold can be calculated for memantine.
Journal Article↗
Gamma activity in the piriform cortex and behavioral thresholds for electrical stimulation in the olfactory bulb.
The olfactory bulb was stimulated by trains of electrical pulses in freely moving rats. Evoked responses resembling damped oscillations at the gamma frequency of 30-60 Hz were recorded in the anterior and posterior piriform cortex. Different types of unconditioned sniffing were induced by stimulation of the olfactory bulb. They were similar to those evoked by an odorant (amylacetate) but differed from the behavioral patterns evoked by non-olfactory (auditory) stimulation. Rats were trained to avoid foot-shocks following electrical pulses into the olfactory bulb as conditioned stimulus in a two way shuttle-box paradigm. Threshold electrical intensities for inducing evoked responses in piriform cortex, unconditioned behavior, and learned avoidance were compared. Thresholds for unconditioned and conditioned behavior were significantly higher in comparison with those for evoking gamma discharges in anterior and posterior piriform cortex. The results suggest that fast time-locked synchronization in the gamma range in the piriform cortex induced by synaptic input from theolfactory bulb is not sufficient for inducing corresponding behavior. Thus behavioral detection and probably also olfactory recognition do not seem to be direct consequences of this fast time-locked neural synchronization. Additional neuronal processes that are connected with further elevation of stimulation intensity seem to be necessary for that.
Animals↗
[The effect of a deficiency of the hormones of the peripheral endocrine glands on behavioral, learning and memory processes].
A comparative study of the effects of thyroid, adrenal, and gonadal deficit on capability for learning, retention of memory traces, and behavior was carried out in male rats under conditions of hormonal disbalance produced by extirpation of the endocrine glands. Behavior of animals was tested during the active and passive avoidance learning and in the open field. It was found out that the extirpation of the peripheral endocrine glands impairs learning and reproduction of the acquired reaction and alters the behavior. The results suggest that corticosteroid hormones take part in learning and behavior. Gonadal and thyroid hormones appear to exert a modulating influence on the higher nervous activity.
Adrenal Cortex Hormones↗
Lack of lead effects on fetal development and offspring learning when combined with alcohol in the Long-Evans rat.
Two studies were conducted to evaluate the interactive effects of alcohol and lead during pregnancy in rats. Our purpose was to see if lead, as lead acetate, would influence the alcohol effect already known to exist. In the first study, pregnant Long-Evans rats received lead (as lead acetate), alcohol (20% w/v), or lead plus alcohol once a day on gestation days (GD) 10-20. On GD 20, when animals were sacrificed, mean blood alcohol levels were consistently higher for the lead-plus-alcohol-dosed groups compared to alcohol alone, but these two groups did not differ in maternal weight gain, percent resorptions, litter size, or fetal weight. Mean blood lead levels were not consistently higher in the lead-plus-alcohol groups compared to lead only, but the lead-plus-alcohol groups differed significantly from the lead-only groups at higher doses in the previously mentioned parameters. The lead-only groups did not differ from vehicle controls in any parameter in spite of blood lead levels as high as 300 micrograms/dl. In the second experiment, animals given a combination of alcohol and lead did not differ in activity, passive avoidance, or active avoidance learning compared to animals given alcohol or lead alone. Animals given lead only or the combination of lead plus alcohol had longer first trial latencies in the passive avoidance test. The data indicate that neither lead nor alcohol attenuates or potentiates each other's effects on reproduction or learning behavior in the Long-Evans rat even at high blood lead levels.
Animals↗
Escape and avoidance as responses learned to a specific conflict-produced drive.
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Animals↗
SCRAMBLE PATTERNS AND ESCAPE LEARNING.
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Avoidance Learning↗
Learning: classical and avoidance conditioning the mollusk Pleurobranchaea.
Naive specimens of the marine gastropod Pleurobranchaea withdraw from tactile stimulation of the oral veil and show feeding responses to food chemicals. Experimental subjects, trained by pairing touch (conditioned stimullus) with food chemicals (unconditioned stimulus), soon acquired a classically conditioned feeding response to touch alone. Control subjects that received touch alone or unpaired touch and food chemicals showed significantly fewer feeding responses to touch than did experimentals. Classically conditioned specimens were used for avoidance conditioning. Subjects that received aversive electrical stimulation when they did not withdraw from touch rapidly learned to withdraw rather than to feed in response to touch alone. Controls that received touch alone or unpaired touch and shock continued to exhibit the feeding response to touch alone. The learned responses persisted for up to 2 weeks without reinforcement before extinction, and could be demonstrated in the isolated nervous system.
Animals↗
Inhibitory avoidance and appetitive learning in aged normal mice: comparison with transgenic mice having elevated plasma growth hormone levels.
Groups of 25-month-old ("old") B6C3 hybrid male mice, 6-month-old ("young") normal males, and their age-matched transgenic (TG) siblings overexpressing the bovine growth hormone gene were given an inhibitory avoidance training trial (0.20-mA electric shock, 1.0-s duration). The old B6C3 hybrids and the young TG mice displayed poorer retention (shorter latencies to enter the shock compartment) 24 h and 42 days after training than did the young normal mice. In a subsequent multiple-trial acquisition test, young TG and old normal mice required more trials to reach the criterion of complete inhibition of step-through responding for 300 s than did young normal mice. Young normal and young TG mice did not differ in trials to extinction, but TG mice met the extinction criterion sooner than did old normal mice, suggesting poorer longterm retention. In tests of T-maze appetitive learning, young normal, old normal, and young TG mice did not differ in acquisition or 24-h retention. Contrary to expectation, TG mice acquired T-maze reversal learning in fewer trials than did young normal or old normal mice. The TG and young normal mice did not differ in retention when retested 44 days after initial training, but old normal mice showed poorer retention than did the young normals. Results of locomotor activity and shock response tests suggested that learning impairments were not due to differences in locomotor activity or shock response thresholds in these animals. Tests in an elevated plus maze indicated that young TG mice were less anxious in a novel environment than their normal siblings, which may contribute to their impaired inhibitory avoidance learning. These findings suggest that 6-month-old TG mice overexpressing the bovine growth hormone gene display alterations in inhibitory avoidance (but not appetitive) learning similar to those occurring in 25-month-old normal mice. The neurobiological mechanisms mediating inhibitory avoidance and T-maze appetitive learning in these animals may be largely dissociated.
Aging↗
Development switch in neural circuitry underlying odor-malaise learning.
Fetal and infant rats can learn to avoid odors paired with illness before development of brain areas supporting this learning in adults, suggesting an alternate learning circuit. Here we begin to document the transition from the infant to adult neural circuit underlying odor-malaise avoidance learning using LiCl (0.3 M; 1% of body weight, ip) and a 30-min peppermint-odor exposure. Conditioning groups included: Paired odor-LiCl, Paired odor-LiCl-Nursing, LiCl, and odor-saline. Results showed that Paired LiCl-odor conditioning induced a learned odor aversion in postnatal day (PN) 7, 12, and 23 pups. Odor-LiCl Paired Nursing induced a learned odor preference in PN7 and PN12 pups but blocked learning in PN23 pups. 14C 2-deoxyglucose (2-DG) autoradiography indicated enhanced olfactory bulb activity in PN7 and PN12 pups with odor preference and avoidance learning. The odor aversion in weanling aged (PN23) pups resulted in enhanced amygdala activity in Paired odor-LiCl pups, but not if they were nursing. Thus, the neural circuit supporting malaise-induced aversions changes over development, indicating that similar infant and adult-learned behaviors may have distinct neural circuits.
Age Factors↗