"Learned helplessness," "learned hopefulness," and "learned obsessiveness": effects of varying contingencies on escape responding.
Explore the source record for details and available documents.
Conditioning, Operant↗
SEARCH · Search PubMed
Results for “Helplessness, Learned”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
In vivo serotonin release and learned helplessness.
Learned helplessness, a behavioral depression caused by exposure to inescapable stress, is considered to be an animal model of human depressive disorder. Like human depression, learned helplessness has been associated with a defect in serotonergic function, but the nature of this relationship is not entirely clear. We have used in vivo microdialysis brain perfusion to measure serotonin (5-hydroxytryptamine, 5HT) in extracellular space of medial frontal cortex in conscious, freely moving rats. Basal 5HT levels in rats perfused before exposure to tail-shock stress did not themselves correlate with subsequent learned helplessness behavior. However, 5HT release after stress showed a significant increase with helpless behavior. These data support the hypothesis that a cortical serotonergic excess is causally related to the development of learned helplessness.
Animals↗
Psychosocial function following temporal lobectomy: influence of seizure control and learned helplessness.
Learned helplessness is the perception that one's behaviour cannot produce a desired outcome. Individuals with intractable epilepsy who have learned that the occurrence of a seizure is beyond their control can develop such a helpless attitude with cognitive, affective and behavioral components which may generalize to many aspects of life. Post-operative testing was done on 42 patients, aged 17-60 years with I.Q. > 80 who had temporal lobectomies (25 R, 17 L) with follow-up 1-14 years (mean 5 years). In addition to seizure outcome, psychosocial adjustment was measured using the Washington Psychosocial Inventory (WPSI) and a structured interview. Three variables of learned helplessness were also assessed: internal or external locus of control, resourcefulness, and depression. Seizure outcome was: completely seizure free, 36%; > 90% improvement, 38% < 90% improvement, 26%. Overall post-operative psychosocial adjustment was good, marked improvement in lifestyle was noted by 85%, personality change for the better by 65% and improved mood by 47%. A transient mood disorder was noted by 38% in the first six months following surgery. Psychosocial adjustment was better in patients who were seizure free or had > 90% reduction in seizures compared to those with < 90% improvement. Two measures of learned helplessness, depression and lack of resourcefulness correlated with poor postoperative psychosocial adjustment. Other variables beside seizure control must be considered in determining the ultimate outcome of epilepsy surgery.
Adaptation, Psychological↗
Learned helplessness and learned resourcefulness: effects of noncontingent success and failure on individuals differing in self-control skills.
We designed two experiments to investigate the role of self-control processes in learned-helplessness studies by assessing the differential reactions to uncontrollability of subjects who presumably had either a rich (high resourceful, or HR) or poor (low resourceful, or LR) repertoire of self-control skills. HR and LR subjects received noncontingent success feedback, failure feedback, or no feedback on a task that ostensibly assessed "therapeutic abilities." Subjects were subsequently tested on insolvable puzzles (Experiment 1) or on solvable anagrams (Experiment 2). According to Kanfer and Hagerman's (1981) self-regulation model, self-regulatory activities are evoked primarily in situations in which subjects are faced with repeated failure. Hence we predicted that individual differences in self-control would influence performance on the insolvable puzzles and not anagram performance after exposure to noncontingent failure. This prediction was confirmed: Only the performance of LR subjects on the insolvable puzzles was debilitated by the helplessness induction, whereas HR and LR subjects showed equal helplessness-induced deficits on the anagrams. The latter finding was interpreted in terms of the learned-helplessness model without the mediating effects of self-regulatory processes. As predicted from the self-control model, HR subjects more frequently checked statements indicating positive self-evaluations and task-oriented thoughts and less frequently checked negative self-evaluations than did LR subjects during exposure to uncontrollability in both experiments. We concluded that the self-control model accounts best for subjects' self-reactions during exposure to uncontrollability or failure, whereas the learned-helplessness model accounts for the generalization of helplessness from uncontrollable situations to controllable ones.
Environment↗
Learned helplessness and learned effectiveness: effects of explicit response cues on individuals differing in personal control expectancies.
Female undergraduates (n = 62) who scored as extreme internals or externals on the Mirels Personal Fate Control Scale participated in a partial replication of Hiroto's learned helplessness experiment. Lights were added to the treatment apparatus, which made explicit to subjects the contingency or noncontingency between their responses and the termination of an aversive tone. As predicted, the performance of internals was significantly impaired by uncontrollability (learned helplessness), while that of externals was facilitated by controllability (learned effectiveness). Externals performed as well as internals in the "escapable" condition, but their performance was inferior to that of internals in the control condition. Following "inescapable" treatment, internals performed worse than externals. These results are supportive of Lefcourt's theory of cue explication. Implications for locus of control and learned helplessness research are discussed.
Acoustic Stimulation↗
Stock differences in the susceptibility of rats to learned helplessness training.
Learned helplessness (LH) consists of shock escape deficits evidenced by animals previously exposed to inescapable shock. This phenomenon has shown promise as a behavioral screen for new antidepressant drugs. Unfortunately, some stocks of rats evidence low susceptibility to LH training. Accordingly, male rats from 8 different stocks were tested for susceptibility to LH training. The outbred stocks consisted of Harlan SD, Sasco Holtzman, and Charles River Holtzman. The inbred stocks (i.e. strains) tested were Lewis, Wistar Kyoto, Brown Norway, Fischer F-344, and Buffalo. The Lewis, Brown Norway, Fischer and Sasco Holtzman rats were found to be virtually non-susceptible to LH training. Harlan SD and Buffalo rats evidenced intermediate susceptibilities of 28% and 33%, respectively. Kyoto and Charles River Holtzman rats were the most susceptible at 53% and 55%, respectively. No stock differences between control animals were observed. These results indicate that wide differences in susceptibility to LH training exist in rats from different stocks or suppliers and researchers should be careful to choose subjects from a susceptible stock. Charles River Holtzman and Wistar Kyoto rats appear to be very susceptible to LH training.
Animals↗
Increased 5-HT2 receptor-mediated behavior 11 days after shock in learned helplessness rats.
In the learned helplessness procedure, rats can be differentiated into two distinct groups. Learned helplessness (LH) rats do not learn to escape a controllable shock while non-learned helplessness (NLH) rats learn this response. This deficit in performance in LH rats lasted for 11 days. In LH rats, pretreatment with acute desipramine (15 mg/kg i.p.) or chronic diazepam (0.95 mg/kg/day p.o. for 7 days) did not produce recovery from this deficit of performance, but pretreatment with chronic desipramine (17.7 mg/kg/day p.o. for 7 days) or chronic mianserin (6.1 mg/kg/day p.o. for 7 days) led to recovery. Before presentation of uncontrollable shock, there was no difference between LH and NLH rats, but 11 days after the shock, head shakes induced by (+/-)-1-(2,5-demethoxy-4-iodophenyl)-2-aminopropane (DOI) in LH rats was significantly more frequent than those in NLH and naive rats without change of [3H]ketanserin binding. The basal corticosterone level was higher in LH rats than in NLH rats. These findings suggest that the learned helplessness model is a reliable animal model of depression accompanied by 5-HT2 receptor hypersensitivity.
Animals↗
Learned helplessness.
1. Nurses described learned helplessness solely in terms of residents not performing the daily activities they were capable of. 2. The relatively strong correlation between the learned helplessness subscale of the MDI and the Beck Depression Inventory suggests that learned helplessness can be maladaptive and dysfunctional. 3. Analysis of attributional style found that personal, stable, and global attributions for negative events were closely associated with LH scores and self-reported depressive symptomatology in this sample. 4. Residents, except in the areas of meals and privacy, generally reported satisfaction with the amount of control they had in their treatment setting.
Aged↗
Learned helplessness: the role of individual differences in learned resourcefulness.
The term 'learned resourcefulness' refers to an acquired repertoire of behaviours and skills by which a person self-regulates internal events (such as emotions, pain, and cognitions) that interfere with the smooth execution of a target behaviour. Sixty undergraduate students were rated as either high resourceful (HR) or low resourceful (LR) according to their scores on Rosenbaum's Self-Control Schedule. Subjects were then pre-treated with inescapable, escapable or control aversive tone followed by anagram solution testing. As hypothesized the learned helplessness phenomenon, the interference with new learning following inescapable aversive events, appeared only in LR subjects and not in HR subjects. No relationship was found between subjects' causal attributions for their performance on the noise task and their subsequent performance on the anagrams as would be predicted from the attributional part of the recent reformulation of the learned helplessness model. It was concluded that subjects' general repertoire of self-control skills, and their general expectations for self-efficacy, might be at least as important in explaining the generalization of helplessness from the training task to the test task as the kinds of causal attributions subjects make for their performance on the training task.
Adaptation, Psychological↗
Hippocampal neuropeptide Y mRNA is reduced in a strain of learned helpless resistant rats.
The learned helpless rat is considered to be one of the better animal models of depression. A genetically inbred strain with a high vulnerability to develop helplessness (LH), as well as a highly resistant strain (NLH) have both been developed. Since the brain peptide neuropeptide Y (NPY) is involved in the regulation of a number of behaviors known to be altered in clinical depression as well as in learned helplessness, we measured the relative level of NPY mRNA in the hippocampus and cortex of control Sprague Dawley (SD), LH and NLH rats. We find that NLH rats have approximately a 30-35% decrease in basal hippocampal NPY mRNA compared with SD and LH rats. By contrast, cortical NPY mRNA and hippocampal pre-proenkephalin and somatostatin mRNA levels were not significantly different in the 3 strains. The data suggest that the regulation of NPY gene expression may be involved in the reduced vulnerability of NLH rats to develop learned helplessness.
Amino Acid Isomerases↗
A comparative approach to the behavior called "learned helplessness'.
The phenomenon of 'learned helplessness' is seen broadly across the animal kingdom. The basic characteristics of this behavior are similar in intact mammals, lower vertebrates and invertebrates. In fact, the basic characteristics even are seen in an isolated thoracic ganglion of an insect. The brain is evidently not essential either in mammals or in invertebrates for demonstrating this behavior. A neutral terminology is suggested that allows for investigation of this behavior and its underlying mechanisms in both intact and surgically simplified preparations of both vertebrates and invertebrates. Thus, its phylogeny can be investigated. In addition, simpler systems such as the insect ventral nerve cord with its large neurons and its ease of pharmacological manipulation may have important contributions to make to understanding the neuropharmacology underlying it. The ubiquity of the phenomenon in different phyla suggests that while in the laboratory it may appear maladaptive, this may not necessarily be the case in a natural ecological context. Because of increasing governmental regulations in both Europe and the US on mammalian studies involving shock and distress, such as that associated with 'learned helplessness', it may be prudent to consider other systems that may offer insight into its underlying mechanisms.
Adaptation, Psychological↗
Effects of bilateral adrenalectomy on the induction of learned helplessness behavior.
In the learned helplessness model of depression, naive Sprague-Dawley rats are exposed to a 40-minute uncontrollable shock training and are subsequently tested in a shock escape paradigm. "Helpless rats" exhibit 11 to 15 failures in a 15-trial test while "nonhelpless" rats and naive controls score 0 to 5 failures in the same test. We report on the effect of bilateral adrenalectomy on the induction of learned helplessness. Most of the adrenalectomized rats (70%) became helpless whereas sham controls responded to the training and testing similarly to naive nonoperated rats (20% to 30% helpless). This increase in behavioral deficits after adrenalectomy was reversed by administration of corticosterone, the naturally occurring glucocorticoid in rat. We conclude that secretion from the adrenal cortex is necessary for the incorporation of a learned response after stress and that a dysregulation of the hypothalamic-pituitary-adrenal axis seems to be involved in helpless behavior.
Adrenalectomy↗
Learned helplessness at work.
The development of theory and research on learned helplessness is reviewed and criticized on some points, e.g., for its reliance on artificial laboratory experiments. Some empirical findings are presented, indicating a connection between certain work characteristics and learned helplessness. Other research traditions have emphasized the importance of job qualifications, freedom of action, and development possibilities for well-being and health. There is, however, hardly and research on learned helplessness at work. Learned helplessness hypotheses should be tested on data from real life; if applied to work environment research, the theory of learned helplessness could generate important results.
Achievement↗
Effects of the antiglucocorticoid RU 38486 on the induction of learned helpless behavior in Sprague-Dawley rats.
Learned helplessness (LH) is induced by exposure to an inescapable or uncontrollable stressor which results in an inability to escape or avoid the same stressor when subsequently presented in a different context. In order to understand which central mechanisms may influence the expression of the learned helpless phenotype, we have pursued an experimental approach that seeks to elucidate the behavioral effects of glucocorticoid (GC) hormones in this animal model of depression. We have previously shown that the induction of LH behavior is enhanced by adrenalectomy, an effect that is reversed by corticosterone. In this study, our aim was to attempt to locate CNS sites responsible for the observed effects of glucocorticoids on learned helpless behavior by introducing the type II GC receptor antagonist, RU 38486 to discrete brain regions. We did not observe a significant effect in LH with acute systemic, acute dentate gyrus or intracerebroventricular injection of RU 38486 in contrast to previous studies using the Porsolt swim test, another animal model of depression. However, we were able to observe a significant change upon chronic administration to the dentate gyrus. These findings suggest that glucocorticoids exert a long-term influence on stress-induced behavior, presumably by affecting glucocorticoid responsive genes in the dentate gyrus.
Animals↗
Effect of beta-adrenergic and serotoninergic agents on the stress-induced behaviour of "learned helplessness" in rats.
The phenomenon of "learned helplessness" is characterized by elements of motor, cognitive and emotional deficit, and it is particularly suitable to be used as a "model" of behavioural depression. There is no doubt about the central role of the cerebral noradrenaline and serotonin in the stress-induced behavioural deficit. The effects of two known beta-adrenoceptor agonists--salbutamol and trimetoquinol--and the beta-adrenergic blockers propranolol and compound 3B, with beta-blocking activity equipotent to that of propranolol, were investigated under conditions of "prophylactic" and "therapeutic" administration in rats subjected to stress by modelling of the behaviour of learned helplessness. Among the serotoninergic agents, the effects of 5-hydroxytryptophane and of the inhibitor of serotonin synthesis, parachlorophenylalanine, were studied. The experimental results show a favourable effect on the behavioural deficit, caused by the blocking of the adrenergic transmitter system and by increasing the activity of the serotoninergic system.
Adrenergic beta-Agonists↗
Learned helplessness, depression, and anxiety.
The learned helplessness model of depression predicts that depressives should tend to perceive reinforcement as response-independent in skill tasks. Depressed-anxious, nondepressed-anxious, and nondepressed-nonanxious college students estimated their chances for success in a skill or a chance task. (Virtually no depressed-nonanxious subjects could be obtained.) Depressed-anxious subjects showed less expectancy change in skill than nondepressed-anxious subjects, while these two groups exhibited similar expectancy change in chance. Nondepressed-anxious and nondepressed-nonanxious subjects did not differ in either skill or chance. The results for a discrimination learning problem were mixed. The groups did not differ in latency to shut off an aversive noise. So, depressed subjects perceptually distort the outcomes of skilled responding as being response-independent, and they may, under certain conditions, show deficits at learning the consequences of responses. These deficits may reflect learned helplessness and are specific to depression.
Anxiety↗
Specificity of the learned helplessness model of depression.
The learned helplessness model of depression was tested for its responsiveness to several types of antidepressant therapies, and to a number of psychoactive drugs which are not effective in treating depression in humans. Chronic administration of tricyclic antidepressants (imipramine, desipramine, amitryptyline, nortryptyline, or doxepin), atypical antidepressants (iprindole or mianserin), monoamine oxidase inhibitors (iproniazid or pargyline), or electroconvulsive shock was effective in reversing learned helplessness. Chronic treatment with anxiolytics (diazepam, lorazepam, or chlordiazepoxide), neuroleptics (chlorpromazine or haloperidol) stimulants (amphetamine or caffeine), or depressants (phenobarbital or ethanol) was not. Thus, this model provides a reasonable degree of specificity toward therapies which are successful in humans.
Animals↗
[Analysis of acute and chronic effects of antidepressive agents in a learned helplessness model in mice].
In experimental learned helplessness in mice determined by preliminary inavoidable aversive exposure, activity of tricyclic antidepressants (desipramine, chlorimipramine, amitryptyline), type A MAO inhibitors (pyrazidol), and atypical (zimelidine, trazodon, befuralin) antidepressants as well as that of potential antidepressants (LIS-30, DZK-153) were determined upon chronic administration. The tricyclic compounds, befuralin and DZK-153 removed learned helplessness only after 14 days of administration. The substances with a predominant serotoninomimetic action (zimelidin, trazodon in high doses, pyrazidol, LIS-30) showed high efficacy following 6 days of administration. Single administration of the substances under study did not make it possible to disclose their specific antidepressant activity.
Animals↗