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PubMed2000

Effects of uncontrollability and failure on the development of learned helplessness in perceptual-motor tasks.

The aim of this study was to distinguish between the roles of uncontrollability and failure on learned helplessness in a perceptual-motor task. Forty-eight junior high school students were randomly assigned in a 2 x 2 (Controllability: Contingent vs. Yoked Noncontingent Feedback x Type of Outcome: Success vs. Failure) factorial design to complete a gun-shooting task on a moving target using a computer screen. Twelve other participants (control group) simply read a passage. After filling out causal attribution and self-efficacy expectations questionnaires, all participants carried out another gun-shooting task (test task). Results showed that contingency led to higher performances than noncontingency. Success conditions elicited higher self-efficacy expectations than failure conditions. Failure entailed less persistence than success did for participants who had been assigned to the contingency condition. Internalization of failure was negatively correlated with persistence. Comparisons with the control group showed that expectations and performance deficits of learned helplessness were provoked by failure in noncontingent situations; persistence deficits were due to failure in contingent situations. These results reveal that both uncontrollability and failure can be responsible for different forms of learned helplessness.

Adolescent↗

PubMedDate not supplied

[Learned helplessness and depression in the aged. A study of the concept of Seligman's depression in the old age home].

Seligman's concept of "learned helplessness" is examined with a sample of rest-home residents. A semi-structured interview is used to assess attributions in the dimensions of internality, stability and generality for past, present, and future life-events. Interrelations of these attributions with depression and age-related self-esteem are investigated. According to Seligman's model elderly subjects with high scores in depression and age-related self-esteem tend to attribute negative life-events as internal, stable and global. Some other assumptions of the model of "learned helplessness" could not be confirmed. Methodological problems are discussed with respect to Seligman's theory of learned helplessness and depression in the elderly.

Aged↗

PubMed1998

Antidepressantlike effects of chronic nicotine on learned helplessness paradigm in rats.

BACKGROUND: The association between smoking and depression has been widely investigated. Smoking cessation is known to induce depression to a variable extent, and patients with a history of depression are more likely to experience depressive symptoms. To investigate the hypothesis that nicotine may have an antidepressantlike effect, we used learned helpless rats as an animal model of depression. METHODS: Learned helplessness was produced according to our previous method. Learned helpless rats were implanted with nicotine and escape test was performed at 7 and 14 days after the implantation. RESULTS: The number of escape failure in the rats receiving 1.5 mg/kg/day of nicotine was significantly reduced (p < .05) compared to control at day 14. Furthermore, this effect was blocked when the nicotinic receptor antagonist mecamylamine was coadministered. CONCLUSIONS: These results suggest that chronic nicotine may act as an antidepressant, probably via nicotinic receptors.

Animals↗

PubMedDate not supplied

Indices of brain beta-adrenergic receptor signal transduction in the learned helplessness animal model of depression.

Both stress response and antidepressant drug action may be mediated by beta-adrenergic receptors (beta AR). Since learned helplessness is a stress-induced animal model of depression, beta AR are relevant to investigate in this model. To date, studies have measured changes in total receptor density (RT), but have not examined more detailed aspects of signal transduction mechanisms such as coupling of the receptor to GS protein. We have investigated brain beta AR coupling in the frontal cortex, hippocampus and hypothalamus of rats exposed to inescapable shock and then tested for learned helplessness, and in both tested and naive controls using [125I]-iodocyanopindolol (ICYP) as the ligand. Both antagonist-saturation and agonist-displacement experiments were conducted, and the specificity for the beta AR was optimized by excluding ICYP binding to 5HT1B receptors. The percentage receptor density in the high-conformational state (%RH) and the ratio of agonist (isoproterenol) dissociation constant from the receptor in the low-/high-conformational states (KL/KH) were used as indices of coupling to GS protein. No significant differences were found between rats developing learned helplessness and non-helpless rats after inescapable stress in any parameter measured in any brain region. In the frontal cortex, exposure to inescapable shock induced beta AR uncoupling from GS protein as suggested by a low KL/KH ratio both in helpless and non-helpless rats but not in either control group. In the hypothalamus, there were trends for higher RL, RT and KL/KH ratio in helpless rats and stressed controls compared to naive controls. These findings suggest that beta AR binding parameters in frontal cortex, hippocampus or hypothalamus did not differentiate between helpless and non-helpless rats. Changes in beta AR coupling observed in these brain regions may reflect effects of stress, which appeared to be region-specific, rather than stress-induced behavioral depression.

Adrenergic beta-Antagonists↗

PubMed1981

GABAergic modulation of learned helplessness.

Previous studies have demonstrated the GABAergic system in the hippocampus to be a major controlling factor in the reversal of learned helplessness by antidepressants. In the present work, animals in which learned helplessness (LeH) was induced by exposure to uncontrollable electric shock demonstrated a decreased depolarization-induced release of GABA relative to controls, and an increased release of hippocampal glutamate. Injection of bicuculline but not glutamate into the hippocampus produced a behavioral state identical to that induced by uncontrollable shock, but had no influence on pain sensitivity. When flux through the "small" hippocampal pool of GABA was determined, chronic treatment with imipramine or iprindole, but lorazepam or chlorpromazine elevated this measure. These three findings along with those of prior experiments, suggest a controlling role for GABA in the learned helplessness model of depression.

Amino Acids↗

PubMed1984

Learned helplessness: effects of noncontingent reinforcement and response cost with emotionally disturbed children.

In order to investigate the effectiveness of noncontingent reinforcement and response cost in inducing learned helplessness and to determine whether depressed Ss respond differently than nondepressed Ss, 28 emotionally disturbed children (20 boys, 8 girls) were tested in a modified learned helplessness paradigm. Children's Depression Inventory score and diagnosis were each used to distinguish "depressed" and "nondepressed" children. Half of the depressed group and half of the nondepressed group received noncontingent response cost, the other half of the two groups received noncontingent positive reinforcement. Results indicated that both noncontingent response cost and noncontingent reinforcement led to reduced persistence time relative to persistence under conditions of contingent reinforcement. There was only one significant difference between depressed and nondepressed Ss (differential persistence time over trials) and there were no significant interactions. Results were discussed in terms of Seligman's formulation of learned helplessness and the extension of this model to a clinical child population.

Achievement↗

PubMed1998

Antidepressant-like effects of alnespirone (S 20499) in the learned helplessness test in rats.

The effects of the new chroman derivative, alnespirone (S 20499), which is a selective 5-HT1A receptor agonist, were investigated in an animal model of depression, the learned helplessness test. Rats previously submitted to a session of 60 inescapable electric foot shocks (learned helpless controls) exhibited a deficit in escape performance in three subsequent shuttle-box sessions. Alnespirone was administered twice daily via the oral route (2.5, 5, 10, 20 mg kg(-1) day(-1)). It was shown to protect against the elevation in escape failures caused by exposure to the uncontrollable aversive situation at 5 and 10 mg kg(-1) day(-1) p.o. (13+/-2 and 10+/-3 escape failures, respectively, vs. 9+/-2 escape failures in control rats). In addition, alnespirone had a tendency to elevate the number of intertrial crossings during the resting periods, depending on the dose and day on which the avoidance task was performed (15+/-2 intertrial crossings at the dose of 5 mg kg(-1) day(-1), vs. 5+/-2 intertrial crossings for the helpless control rats, on the second day). In comparison, imipramine (64 mg kg(-1) day(-1) p.o.) provided marked protection on all three days of the avoidance task and tended to increase the number of intertrial crossings during the resting periods on the second and the third days. It is concluded that alnespirone exerts antidepressant-like properties in the learned helplessness test in rats, in a manner similar to 8-OH-DPAT (8-hydroxy-2-(di-n-propylamino)tetralin), buspirone and ipsapirone, other 5-HT1A receptor agonists.

Animals↗

PubMed1982

Evidence for a serotonergic mechanism of the learned helplessness phenomenon.

The present experiments examined the role of the serotonergic system in the learned helplessness phenomenon. In Experiment 1, a 200 mg/kg dose of 1-tryptophan injected 30 min prior to testing disrupted acquisition of Fixed Ratio 2 shuttle escape behavior. In Experiment 2, a 100 mg/kg dose of 5-HTP produced interference with the acquisition of the escape response. Furthermore, this interference was prevented by treatment with the serotonergic antagonist methysergide. In Experiment 3, animals were pretreated with a subeffective dose of 1-tryptophan in combination with subeffective exposure to inescapable shock. These animals showed a deficit in the acquisition of FR-2 shuttle escape. In Experiment 4, combined exposure to a subeffective dose of 5-HTP and inescapable shock (40 trials) resulted in an acquisition deficit. This deficit was reversed by methysergide. Experiment 5 showed that the detrimental effects of exposure to prolonged (80 trials) of inescapable shock can be prevented by treatment with methysergide. These studies implicate the serotonergic system as a possible mediator of the learned helplessness phenomenon.

Animals↗

PubMed1998

The effect of oxcarbazepine on behavioural despair and learned helplessness.

The effect of oxcarbazepine was evaluated in two tests of depression (forced swimming and learned helplessness) and in the open-field test. Acute (three times over 24 h) oxcarbazepine 80 mg/kg (but not 40 mg/kg) decreased immobility time in the forced swimming test. In the learned helplessness test, 4 days of treatment with oxcarbazepine 80 mg/kg reversed the deficits induced by foot-shock in rats submitted to the two-way active avoidance test. Oxcarbazepine 80 mg/kg did not modify the behaviour of rats in the open-field test, an indication that, at this dose, oxcarbazepine did not show a locomotor stimulatory effect. Thus, the data of the present study suggest that oxcarbazepine has a potential antidepressive effect.

Animals↗

PubMed2001

The influence of gender and the estrous cycle on learned helplessness in the rat.

Although the etiology of clinical depression is unknown, women are more likely to suffer from major depressive disorder than men. In addition, in some women, there is a clear association between depression and specific phases of the menstrual cycle. Surprisingly little research has examined gender differences and the influences of the estrous cycle in this and other animal behavioral models of clinical depression. Learned helplessness is a valid animal model of stress-induced behavioral depression in which prior exposure to inescapable stress produces deficits in escape testing. Learned helplessness was studied in rats using an inescapable tail shock stress followed by a shuttle box test to determine escape latencies. Animals with mean escape latencies of >or=20 s after shuttle-box testing are defined as learned helpless. Males and normal cycling female rats in the estrus and diestrus II phases were studied. Female rats in the diestrus II phase had significantly higher escape latencies and exhibited a more helpless behavior than female rats in the estrus phase. Male rat escape latencies were intermediate between the two female phases. These results suggest a role for gonadal hormones in the development of stress-induced behavioral depression or 'learned helplessness.'

Animals↗

PubMed1984

Learned helplessness and animal models of depression.

The degree to which organisms can exert control over events to which they are exposed has a strong impact on behavior and physiological functioning. Effects caused by the uncontrollability of events that are beyond the organism's control rather than by the events per se have been called learned helplessness effects. The present paper reviews such learned helplessness effects. At a behavioral level, uncontrollable aversive events result in associative, motivational, and emotional deficits. At a neurochemical level, uncontrollable but not controllable aversive events have been reported to lead to disturbances in cholinergic, noradrenergic, dopaminergic, serotonergic, and GABAergic systems. However, there are interpretive difficulties in this literature, and these are discussed. The controllability/uncontrollability of aversive events has a role in producing stress-induced analgesia and the activation of endogenous opiate systems. These relationships are reviewed. It is proposed that the learning that aversive events cannot be controlled activates an opiate system. The research reviewed is related to depression, and the general issue of animal models of depression is discussed. It is concluded that no experimental paradigm can be a model of depression in some general sense, but can only model a particular aspect. Learned helplessness may model "stress and coping".

Affect↗

PubMedDate not supplied

A computerized system for learned helplessness experiments.

A microcomputer-based system for carrying out learned helplessness experiments is described. The hardware is inexpensive and easily available. The program is written in BASIC and must be executed in the compiled form in order to keep up with real-time events. It contains an algorithm for calculating inter-trial intervals and allows the experimentor to freely select experimental conditions such as duration of shock, number of trials, etc. The task that the rat is required to do to stop the shock is also selectable, thus giving the experimentor the opportunity to maximize behavioral differences between escapable and inescapable rats while these differences are being induced. Experimental data on 12 rats that went through this automated protocol are analyzed and discussed.

Analysis of Variance↗

PubMed2006

Methylene blue facilitates the extinction of fear in an animal model of susceptibility to learned helplessness.

The objectives were to (1) extend previous findings on fear extinction deficits in male congenitally helpless rats (a model for susceptibility to learned helplessness) to female congenitally helpless rats, and (2) attempt a therapeutic intervention with methylene blue, a metabolic enhancer that improves memory retention, to alleviate the predicted extinction deficits. In the first experiment, fear acquisition (four tone-shock pairings in operant chamber) was followed by extinction training (60 tones in open field). Congenitally helpless rats showed fear acquisition similar to controls but had dramatic extinction deficits, and did not display the gradual extinction curves observed in controls. Congenitally helpless rats demonstrated greater tone-evoked freezing as compared to controls in both the acquisition and extinction contexts one week after extinction training, and also in the extinction probe conducted one month later. In the second experiment (which began one month after the first experiment) congenitally helpless subjects were further exposed to tones for 5 days, each followed by 4 mg/kg methylene blue or saline IP, and had a fear renewal test in the acquisition context. Methylene blue administration improved retention of the extinction memory as demonstrated by significant decreases in fear renewal as compared to saline-administered congenitally helpless subjects. The impaired ability to extinguish fear to a traumatic memory in congenitally helpless rats supports the validity of this strain as an animal model for vulnerability to post-traumatic stress disorder, and this study further suggests that methylene blue may facilitate fear extinction as an adjunct to exposure therapy.

Analysis of Variance↗

PubMed1984

Attributional style and the generality of learned helplessness.

According to the logic of the attribution reformulation of learned helplessness, the interaction of two factors influences whether helplessness experienced in one situation will transfer to a new situation. The model predicts that people who exhibit a style of attributing negative outcomes to global factors will show helplessness deficits in new situations that are either similar or dissimilar to the original situation in which they were helpless. In contrast, people who exhibit a style of attributing negative outcomes to only specific factors will show helplessness deficits in situations that are similar, but not dissimilar, to the original situation in which they were helpless. To test these predictions, we conducted two studies in which undergraduates with either a global or specific attributional style for negative outcomes were given one of three pretreatments in the typical helplessness triadic design: controllable bursts of noise, uncontrollable bursts of noise, or no noise. In Experiment 1, students were tested for helplessness deficits in a test situation similar to the pretreatment setting, whereas in Experiment 2, they were tested in a test situation dissimilar to the pretreatment setting. The findings were consistent with predictions of the reformulated helplessness theory.

Adult↗

PubMed1989

Effects of ipsapirone and BAY R 1531 on learned helplessness.

The effects of the 5-hydroxytryptamine-1A (5-HT1A) receptor agonists on the learned helplessness test were investigated. Rats were submitted to a single session of 60 uncontrollable shocks (10-s duration, 1.0 mA, every 60 +/- 40 s) and then treated twice daily with ip injections of either ipsapirone (13 mg/kg daily) or BAY R 1531 (0.375 mg/kg daily) for four consecutive days. On the last day, the animals were submitted to an escape test. The results showed that both drug treatments blocked the deficit in the escape learning (helplessness effect). These data suggest that drugs which stimulate 5-HT1A receptors have an antidepressant-like activity in this animal model of depression.

Animals↗

PubMedDate not supplied

Serotonin and learned helplessness: a regional study of 5-HT1A, 5-HT2A receptors and the serotonin transport site in rat brain.

Serotonin (5-HT) plays a central role in the neurochemistry of the learned helplessness animal model of depression. Using quantitative autoradiography, we measured the density of 5-HT1A and 5-HT2A receptors and of 5-HT transport sites in medial prefrontal cortex, dorsal hippocampus, septum, hypothalamus, and amygdala in learned helpless rats, and in rats that were nonhelpless after inescapable stress, as well as in shuttlebox-tested and nonhandled controls. We found no changes in 5-HT1A receptor density among the groups in any region studied. In dorsal hippocampus, 5-HT2A receptor density was decreased in nonhelpless rats, while in amygdala 5-HT2A receptor density was decreased in both groups of stressed rats, whether helpless or nonhelpless. In the hypothalamus 5-HT2A receptor density, was decreased in helpless rats as compared to controls. In medial prefrontal cortex, the serotonin transport sites showed decreased density in helpless rats as compared to controls but not to nonhelpless rats. These findings further highlight the complexity of regional 5-HT effects in the learned helplessness animal model.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1995

Effects of the beta-adrenergic blockers propranolol and acebutolol on stress-induced learned helplessness behavior of rats.

The latency time and escape ability of rats with learned helplessness behavior were studied after 1, 6 and 14 days of oral treatment with beta-adrenergic blockers propranolol (1 and 3 mg/kg) and acebutolol (10 and 30 mg/kg). A dose-dependent significant decrease in latency time and increase in number of avoidances was established after single, 6 and 14 days propranolol treatment. The selective beta 1-blocker acebutolol did not change the escape characteristics. These results suggest a greater impact of beta 1- than beta 2-adrenergic receptors for escape performance after unescapable foot shock, i.e., learned helplessness behavior.

Acebutolol↗

PubMed1984

Learned helplessness: effects on brain monoamines and the pituitary-gonadal axis.

The effect of the learned helplessness paradigm, a model of depression, on biogenic amines in eight brain regions, and on the serum levels of luteinizing hormone, corticosterone, and testosterone in male rats was determined. Rats which were exposed to uncontrollable and unpredictable shocks (HY-rats) had hormone levels similar to those in appropriate control animals. However, HY-rats had higher levels of 5-HIAA in the pons/medulla oblongata and lower levels of 5-HT in the cortex than rats which could escape the shocks (HE-rats). Furthermore, striatal levels of NE were higher in HY-rats when compared to HE-rats and non-shocked controls (HC-rats). Shock treatment per se resulted in lower NE levels in the hippocampus. These data implicate the serotonergic and noradrenergic systems as possible mediators of the learned helplessness phenomenon, but do not support the view that this behavior is associated with impaired pituitary-gonadal function.

3,4-Dihydroxyphenylacetic Acid↗