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PubMed1991

Nicotine improves cognitive disturbance in rodents fed with a choline-deficient diet.

The effect of nicotine on learning disturbances was tested in rats. Rats were fed either a choline-enriched or a choline-deficient diet. Concentration of acetylcholine in the whole brain was significantly lower in rats fed with choline-deficient diet than rats fed with choline-enriched diet. Passive avoidance learning shows that rats on a choline-deficient diet showed significantly impaired learning compared to rats on a choline-enriched diet. Nicotine (0.04 mg/kg) administered intraperitoneally significantly potentiated learning in rats on a choline-deficient diet, as well as in rats on a choline-enriched diet. We, therefore, suggest that nicotine may potentiate learning in an acetylcholine-deprived brain.

Acetylcholine↗
PubMed1993

Intertrial responses in defensive instrumental learning.

Data by the author, as well as from other laboratories, show residual fear as the main source of intertrial responses (ITR) during defensive instrumental training in rats, cats and dogs. Between-subject differences in ITR rate arise in the course of training. The differences depend on training conditions and on subject's emotionality. Under the same conditions higher ITR rates correspond to more rapid avoidance learning. The increase of ITR rate is regularly observed in the following circumstances: at early stages of training, after transfer to a less salient discriminative stimulus, and after a change of the task requirements. The decrease of ITR rate corresponds to the plateau level of avoidance or escape performance. Both a lower ITR rate and reduced flexibility of behavior are found after lesions of the amygdala nuclei.

Aggression↗
PubMed1989

Repeated failure: a source of helplessness or a factor irrelevant to its emergence?

We tested the validity of the egotism model of human helplessness. In contrast to the original theoretical approach of Seligman and his associates, which points to response-outcome noncontingency as the main source of helplessness, the egotism alternative proposes that repeated failure itself is the critical determinant of helplessness symptoms. Repeated failure threatens the self-esteem of the subject, who supposedly engages in a least-effort strategy during the test phase of a typical learned helplessness study, which results in performance impairment. To examine the egotism explanation, we gave subjects noncontingent-feedback training with or without repeated failure on five consecutive discrimination problems. In two experiments, noncontingent-feedback preexposure produced helplessness deficits in performance on avoidance learning, whereas repeated failure appeared irrelevant to helplessness. This and our other findings from research are inconsistent with the egotism explanation and support instead Seligman's original proposal, in which helplessness is attributed to prolonged experience with noncontingency.

Achievement↗
PubMed1985

Passive avoidance after ibotenic acid and radio frequency lesions in the rat amygdala.

Ibotenic acid (IBO) is assumed to lesion neurons and to spare fibers of passage. The effects of such lesions in the amygdaloid complex of rats were compared to those of radio frequency lesions (RF) on a passive avoidance task. Both lesions impaired the acquisition of the passive avoidance response. Plasma corticosterone levels were measured after a retention test in which no electrical shocks were applied. None of the lesion groups showed reduced corticosterone levels, the IBO lesioned rats actually showed significantly higher corticosterone levels than both RF lesioned and control animals. The corticosterone results are not consistent with a general reduction in fear. The slower avoidance learning may be a conditioning deficit due to impaired sensory information processing in the amygdaloid complex.

Amygdala↗
PubMed1991

Neurochemical mechanisms of chronic antisocial behavior (psychopathy). A literature review.

This article reviews the important emotional correlates of chronic antisocial behavior from the standpoint of primary and secondary psychopathy. Primary psychopaths exhibit a conspicuous lack of empathetic emotions and secondary psychopaths exhibit a conspicuous excess of inappropriate emotions. The article points out the relationship between passive-avoidance learning deficits and primary psychopathy and between central nervous system serotonergic dysfunction and primary and secondary psychopathy.

Adult↗
PubMed2001

Alcohol and behavioral control: cognitive and neural mechanisms.

This article represents the proceedings of a symposium at the 2000 RSA Meeting in Denver, Colorado. The organizer/chair was Muriel Vogel-Sprott. The presentations were (1) Alcohol-induced impairment of inhibitory control: Some commonalities with attention deficit hyperactivity disorder, by Mark Fillmore; (2) Neural interactions that underlie response inhibition under alcohol: A functional magnetic resonance imaging investigation, by Craig Easdon; (3) Intentional control of behavior under alcohol, by Muriel Vogel-Sprott; and (4) Working memory and the disinhibiting effects of alcohol on passive avoidance learning, by Alicia Justius and Peter Finn.

Alcoholism↗
PubMed2004

Cyclin S: a new member of the cyclin family plays a role in long-term memory.

Memory is thought to be subserved by structural and functional alteration in synaptic connectivity. But although neuronal plasticity requires gene expression, the identity of the proteins involved is largely unknown. Using the chick 1-day-old passive avoidance learning paradigm and differential display RNA fingerprinting, we identified 13 candidate genes which are upregulated in the intermediate medial hyperstriatum ventrale (IMHV), an area that has been correlated with the initial processing of memory formation. One of the induced genes is a new member of the cyclin family, with high homology to cyclin L (ania-6a). Analysis of the expression pattern of this gene after training revealed two time waves of induction: the first correlated with learning and initial memory process in the IMHV; the second correlated with memory consolidation, first in the IMHV, and then in the lobus paraolefactoris. There is a correlation between methylanthranilate (MeA) concentrations (the malaise substrate in the passive avoidance training procedure), the duration of memory and the expression level of cyclin S. While training chicks on low concentrations of MeA causes short-term memory and low expression level of cyclin S, high concentration of MeA induces long-term memory and high expression level of cyclin S in the IMHV. The role of cyclins in the regulation of neuronal-plasticity-related gene expression was overlooked, and it might serve as a key step in long-term memory formation.

Amino Acid Sequence↗
PubMed1982

Stereospecificity of behavioural effects of viloxazine in bulbectomized rats does not correlate with its 5-HT-releasing action in vitro.

The effects of the antidepressant drug viloxazine and its two optically active isomers on the passive avoidance learning deficit surgically induced in rats by bilateral bulbectomy have been determined. Fourteen consecutive daily injections of either the racemate or the S-isomer (2, 5 and 10 mg kg-1 i.p.) significantly improved the acquisition of avoidance behaviour. The R-isomer was devoid of such activity in this same dose range. The various isomeric species of viloxazine were also studied in vitro for their ability to induce a release of noradrenaline, dopamine and 5-hydroxytryptamine (5-HT) from rat brain slices. In agreement with previous reports, racemic viloxazine caused a concentration-dependent (10(-5)-10(-3 M) release of 5-MT without affecting any significant change in the release of either catecholamine. However, in contrast to the results of the behavioural studies, this phenomenon did not exhibit stereospecificity, all three isomeric forms being equally active. Thus, there is no simple relationship between viloxazine's behavioural activity in bulbectomized rats and its 5-HT releasing properties observed in vitro. The significance of these findings with respect to previously reported effects of the drug indicative of facilitation of central 5-HT mediated processes is discussed.

Animals↗
PubMed2003

Behavioral patterns under cholinergic control during development: lessons learned from the selective immunotoxin 192 IgG saporin.

The immunotoxin 192 IgG saporin (192 IgG-sap) offers a valuable tool to investigate the role of the developing basal forebrain cholinergic system in modulating behavioral functions in developing, as well as adult rats. After neonatal 192 IgG-sap lesions, rats display reduced ultrasonic vocalizations as neonates, deficits in passive avoidance learning as juveniles, and altered reactions to spatial novelty as adults. These data suggest that neonatal cholinergic depletion affects cognitive performance in juvenile and adult rats. Additionally, neonatal cholinergic depletion alters ultrasonic vocalizations, which could then alter establishing normal mother-infant relationships, and thus compound the pup's cognitive deficits. These findings underscore the importance of assessing behavior during ontogeny, as well as in adulthood.

Acetylcholine↗
PubMed1980

Beta-endorphin causes retrograde amnesia and is released from the rat brain by various forms of training and stimulation.

The endogenous opiate peptide, beta-endorphin (0.4, 1.0, 2.0, and 10.0 microgram/kg) was injected IP into rats immediately after training in a shuttle avoidance task, and its effect on memory retention was evaluated in test sessions carried out 24 h later. The drug was found to cause retrograde amnesia, the ED50 being 1.0 microgram/kg. Beta-endorphin immunoreactivity was measured in the hypothalamus and rest of the brain of rats submitted to training, or test sessions of shuttle avoidance learning, pseudoconditioning in the shuttle-box, tones alone, or foot-shocks alone. After training in any of the four paradigms, there was a marked (46-60%) depletion of beta-endorphin immunoreactivity in the rest of the brain. No changes were detected in the hypothalamus or after test sessions. The loss of beta-endorphin immunoreactivity may be attributed to release of this substance caused by the stimuli used for training. From the present findings, as well as previous observations on the memory-facilitating influence of the opiate receptor antagonist, naloxone, it is concluded that there is a physiological amnesic mechanism mediated by beta-endorphin (and perhaps other opoid peptides as well), which is triggered by the non-associative factors present in the various forms of learning.

Amnesia↗
PubMed1984

Prenatal exposure to morphine in mice: enhanced responsiveness to morphine and stress.

Some behavioral effects of prenatal morphine administration were studied in CD1 mice. Two sets of experiments were carried out. In a first set, which was performed during development: (a) measures of postnatal reflexes revealed only a light deficit in tests involving motor control, (b) activity measures showed a significant reduction of spontaneous activity which was evident only in the course of the first postnatal days. In a second set of experiments, in which adult mice were tested for activity, analgesia and passive avoidance learning: (a) no difference was observed, in baseline conditions, between the performances of the mice prenatally exposed to saline and those preexposed to morphine, (b) as compared with controls, enhanced responsiveness to morphine administration (for the activity and passive avoidance measures), and to morphine and stress (for the analgesic measures) were found.

Analgesia↗
PubMed2003

Design and synthesis of new benzimidazole-arylpiperazine derivatives acting as mixed 5-HT1A/5-HT3 ligands.

A series of new benzimidazole-arylpiperazine derivatives III were designed, synthesized and evaluated for binding affinity at serotoninergic 5-HT(1A) and 5-HT(3) receptors. Compound IIIc was identified as a novel mixed 5-HT(1A)/5-HT(3) ligand with high affinity for both serotonin receptors and excellent selectivity over alpha(1)-adrenergic and dopamine D(2) receptors. This compound was characterized as a partial agonist at 5-HT(1A)Rs and a 5-HT(3)R antagonist, and was effective in preventing the cognitive deficits induced by muscarinic receptor blockade in a passive avoidance learning test.

Animals↗
PubMed1972

Distribution and excretion of N-( 14 C)-methyl labelled m-hydroxybenzyltrimethylammonium ions in mice.

1. Radioactivity in the plasma, livers, and brains of mice was measured at intervals of 10 min to 24 h after the intraperitoneal injection of (14)C labelled m-methoxy- and m-hydroxy- benzyltrimethylammonium ions.2. Well over 10% of the dose of either of these quaternary compounds was found in the liver and plasma within 10 min of the injection, but they were rapidly excreted or metabolized, having a half life of between 1 and 2 hours.3. Small amounts of radioactivity were detectable in brain, and were not due to contamination of brain samples by blood, after doses of 14-16 mumol/kg (approximately 4 mg iodide/kg) and upwards. After doses of 4-6 mumol/kg (approximately 1 mg iodide/kg), however, radioactivity in the brain was barely detectable.4. Any behavioural effects reported to occur in mice treated with these lower doses of m-hydroxybenzyltrimethylammonium, which include improved performance in a test of avoidance learning, are unlikely to be due to an action within the central nervous system. Learning may be more influenced by the peripheral effects of drugs than has hitherto been appreciated.

Animals↗
PubMed1993

A preliminary resolution of the retention of distributed vs massed response prevention in rats.

This study consisted of two experiments conducted to investigate the difference in efficacy and retention of distributed response prevention when compared to massed response prevention using an animal model of avoidance learning. The purpose was to obtain an estimate of the over-all treatment time for response prevention that begins to be affected by the treatment, either distributed or massed. In Exp. 1, 50 rats were given two trials of escape learning in a one-way black-white shuttle-box. Groups received response-prevention treatment or nontreatment in 9 1-min. distributed sessions or 1 9-min. massed session. Subjects were tested using a passive-avoidance paradigm immediately following treatment, 24 hours, and 720 hours (30 days) later. Analysis showed that with an over-all response-prevention time of 9 min., response-prevention treatment was effective in reducing avoidance behavior, that the effect was retained, and that there were no differences between distributed and massed groups. These results led to Exp. II in which 50 rats were exposed to the same training procedure as in Exp. I. These groups received response-prevention treatment or nontreatment in 12 15-sec. distributed sessions or one 3-min. massed session. Analysis of passive-avoidance testing immediately following treatment, 24 hr., and 720 hr. later showed that, when the over-all response-prevention time was 3 min., only groups with distributed treatment showed reduction of avoidance behavior and retention of the treatment effects. Since past studies have produced inconsistent findings in comparing distributed vs massed delivery of response-prevention treatment these two experiments are intended to serve as a preliminary resolution of the past differing results. When the over-all treatment time is longer than 3 min., there is no delivery of treatment effect. However, with 3 min. of over-all treatment time, distributed delivery was necessary to facilitate the treatment effects. Implications for animals and humans are discussed.

Animals↗
PubMed2001

Fornix-dependent induction of hippocampal CCAAT enhancer-binding protein [beta] and [delta] Co-localizes with phosphorylated cAMP response element-binding protein and accompanies long-term memory consolidation.

The cAMP response element-binding protein (CREB) is an evolutionarily conserved transcription regulator essential for long-term memory formation. It is not known, however, whether the molecular events downstream of CREB activation are also conserved. An early, cAMP-dependent event necessary for learning-related long-term synaptic plasticity in the invertebrate Aplysia californica is the induction of the transcription factor CCAAT enhancer-binding protein (C/EBP). Here we show that two homologs in the rat, C/EBPbeta and C/EBPdelta, are induced at discrete times after inhibitory avoidance learning and co-localize with phosphorylated CREB in the hippocampus. This induction is blocked by fornix lesions, which are known to disrupt activation of CREB in the hippocampus and to impair memory consolidation. These results indicate that C/EBPs are evolutionarily conserved components of the CREB-dependent gene cascade activated in long-term memory.

Animals↗
PubMed1984

Effect of bilateral olfactory bulbectomy on discrimination avoidance conditioning in rats.

Studies were made with the two-way shuttle box method on the acquisition of discrimination avoidance learning by olfactory bulbectomized rats in relation to changes in emotional behavior. Bulbectomized rats showed a marked increase in locomotor activity, with accompanying augmentation of the reactivity and the appearance of muricidal behavior. Initially, the bulbectomized rats showed elevated conditioned avoidance responses to both the CS+ and the CS-. In later stages, there was a continued slow increase in responses to the CS+ accompanied by a decrease in responses to the CS-, until responses to both stimuli were only slightly elevated above the levels shown by control rats. This result suggests that olfactory bulbectomy does not affect discrimination ability itself, but the impairment of discrimination during the initial stages is resulted from hyperemotionality induced by olfactory bulbectomy.

Aggression↗
PubMed2005

Prenatal exposure to bisphenol A impairs sexual differentiation of exploratory behavior and increases depression-like behavior in rats.

Perinatal exposure to bisphenol A (BPA, 0.1 and 1 ppm in drinking water applied to mother rats for 6 weeks) has been shown to impair the sexual differentiation in exploratory behavior, but the exact critical period of this disrupting effect is still unknown. In this study, we examined the effects of prenatal exposure to BPA (0.1 ppm in drinking water applied to dams during the final week of pregnant) on emotional and learning behaviors in addition to exploratory behavior. Estimated daily intake was 15 microg/kg/day, below the reference dose (RfD) in the United States and the daily tolerable intake (TDI) in Japan (50 microg/kg/day). The rats were successively tested in open-field test, elevated plus maze test, passive avoidance test and forced swimming test during development from 6 to 9 weeks of juvenile period. Prenatal exposure to BPA mainly affected male rats and abolished sex differences in rearing behavior in the open-field test and struggling behavior in the forced swimming test. BPA increased the immobility of male rats in the forced swimming test. The avoidance learning and behaviors in the elevated plus maze were not affected. The present study demonstrates that male rats at the final week of prenatal period are sensitive to BPA, which impairs sexual differentiation in rearing and struggling behavior and facilitate depression-like behavior.

Animals↗