"Learned helplessness," "learned hopefulness," and "learned obsessiveness": effects of varying contingencies on escape responding.
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Conditioning, Operant↗
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On learned helplessness.
"Learned helplessness" and its Pavlovian analog, learned irrelevance, are phenomena thought integral to understanding depression, PTSD, psychosomatic vulnerability, and a variety of diseases and immune disorders. The origin and development of research on learned helplessness is briefly overviewed with attention to the reasons for the controversy that surrounds the study of learned helplessness and derived physiological, psychological, and behavioral phenomena. The need to remedy past focus on American research and English language journals in this area is noted. The heuristic value as well as the wide ranging empirical value of the research domain is lauded. The meretricious emerging social and legal barriers to this research are noted to be unrealistic and unfortunate.
Animals↗
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 or learned inactivity after inescapable stress? Interpretation depends on coping styles.
Researches on uncontrollable events in the post-soviet states are overviewed. In our research, susceptibility to learned helplessness is studied in rats with active (KHA strain) versus passive (KLA strain) coping styles. Inescapable footshocks, but not escapable footshocks, applied to KHA rats induced escape failures, diminished locomotion and coping, reduced measures of anxiety, and resulted in dexamethasone nonsuppression of the brain-hypothalamus-pituitary-adrenal axis--all characteristic of learned helplessness. In contrast, KLA rats demonstrated the same responses upon exposure to both escapable and inescapable stresses. While learned helplessness occurred in KHA rats, it appears that KLA rats exposed to inescapable stress demonstrated learned inactivity based upon the nondifference between effects of escapable and inescapable shocks. Relationships between coping styles and social ranks are discussed. Our and other's results with genetically selected strains suggest active coping in dominant and subordinate subjects, and passive coping in subdominant animals confirm the importance of coping style and its relation to health under stress.
Adaptation, Psychological↗
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↗
Subchronic treatment with imipramine ameliorates the decreased number in neuropeptide Y-positive cells in the hippocampus of learned helplessness rats.
Learned helplessness, but not immobilization stress, decreased the numbers of neuropeptide Y (NPY)-positive cells (interneuron), but not calcitonin gene-related peptide (CGRP)-positive cells (mossy cell), in the hilus of the hippocampus. Subchronic treatment of learned helplessness rats, but not naive rats, with imipramine ameliorated the decrease in the number of NPY-positive cells. Therefore, NPY-positive cells in the hippocampus may contribute to depression.
Animals↗
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↗
Expression of c-Fos-like immunoreactivity in the brain of mice with learned helplessness.
The learned helplessness (LH) developed after repeat inescapable stress is a well validated animal model of human major depression and is not species specific. c-Fos, the protein product of the protooncogene c-fos, is expressed in neurons under a variety of stressors and could reflect the regional neuronal activation. Using the LH paradigm in mice, we examined c-Fos expression in several brain regions related to stress response or major depression. The LH mice showed significantly lower c-Fos-like immunoreactivity (FLI) in the hippocampus dentate gyrus and the lateral septal nucleus, and higher FLI in the hypothalamic paraventricular nucleus compared with the naive mice. Our finding in the mice LH model supported previous studies in rats showing that the lateral septal nucleus and the hypothalamic paraventricular nucleus are important in LH behaviors. We further demonstrated that hippocampus dentate gyrus, a region important for learning and major depression, may also be involved in the LH behaviors. These related brain regions could provide a basis for further exploration of the molecular mechanisms underlying LH behaviors.
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↗
Differential regulation of serotonin (5HT)2A receptor mRNA and protein levels after single and repeated stress in rat brain: role in learned helplessness behavior.
Stress-induced learned helplessness in animals serves as a model of behavioral depression and other stress-related disorders. Our recent report that repeated stress prolongs the duration of learned helplessness behavior in rats may be important since acute and recurrent disorders may have different responsive mechanisms. To examine the role of serotonergic (5HT) mechanisms in such behavior, we studied the expression of 5HT2A receptors in different brain areas of rats, and further investigated whether the alterations in expression of 5HT2A receptors are similar after single versus repeated stress. Rats exposed to inescapable shock once on day 1, or twice, on day 1 and day 7, were tested for escape latency on days 2 and 4, or day 14, respectively. Higher escape latencies were observed on day 2 after single, and on day 14 after repeated shock. Whereas the single-stress paradigm produced a significant decrease of 5HT2A receptor mRNA and protein expression in hippocampus of non-learned helpless and learned helpless rats as compared with tested controls, repeated stress resulted in increase in frontal cortex but decrease in hippocampus and hypothalamus of learned helpless rats only, as compared with tested control rats. These results demonstrate differential regulation of 5HT2A receptors in LH rats after single and repeated stress, which may be critical in the pathophysiology of depression/other stress-related disorders.
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↗
Increased septal 5-HIAA efflux in rats that do not develop learned helplessness after inescapable stress.
Learned helplessness is a behavioral deficit that can be induced by exposure to inescapable stress. Previous studies have implicated the lateral septum in mediating this phenomenon, and in this brain region, serotonin plays an important role in the development, maintenance, prevention, and reversal of learned helplessness behavior. Using the technique of in vivo microdialysis, we measured the efflux of serotonin (5-HT), dopamine (DA), and their respective metabolites, 5-hydroxyindoleacetic acid (5-HIAA) and 3, 4-dihydroxyphenylacetic acid (DOPAC), from the lateral septum of rats that either developed or did not develop learned helplessness. During the microdialysis session all rats were subjected to restraint stress. Control groups included naïve, home cage rats as well as tested control rats that were subjected to the identical handling, restraint, and shuttlebox testing as the rats that received inescapable shock. Overall, levels of 5-HIAA were significantly higher in non-helpless rats. There were no significant effects of restraint or differences in levels of 5-HT, DA, or DOPAC. We propose that this increase in 5-HIAA is indicative of an overall increase in serotonin metabolism in the lateral septum of rats that do not become helpless after inescapable stress. This increased serotonin metabolism in the lateral septum may protect the animal from adverse behavioral consequences of inescapable stress. J. Neurosci. Res. 61:101-106, 2000. Published 2000 Wiley-Liss, Inc.
3,4-Dihydroxyphenylacetic Acid↗
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↗
Hippocampal synapsin I, growth-associated protein-43, and microtubule-associated protein-2 immunoreactivity in learned helplessness rats and antidepressant-treated rats.
Learned helplessness rats are thought to be an animal model of depression. To study the role of synapse plasticity in depression, we examined the effects of learned helplessness and antidepressant treatments on synapsin I (a marker of presynaptic terminals), growth-associated protein-43 (GAP-43; a marker of growth cones), and microtubule-associated protein-2 (MAP-2; a marker of dendrites) in the hippocampus by immunolabeling. (1) Learned helplessness rats showed significant increases in the expression of synapsin I two days after the attainment of learned helplessness, and significant decreases in the protein expression eight days after the achievement of learned helplessness. Subchronic treatment of naïve rats with imipramine or fluvoxamine significantly decreased the expression of synapsin I. (2) Learned helplessness increased the expression of GAP-43 two days and eight days after learned helplessness training. Subchronic treatment of naïve rats with fluvoxamine but not imipramine showed a tendency to decrease the expression of synapsin I. (3) Learned helplessness rats showed increased expression of MAP-2 eight days after the attainment of learned helplessness. Naïve rats subchronically treated with imipramine showed a tendency toward increased expression of MAP-2, but those treated with fluvoxamine did not. These results indicate that the neuroplasticity-related proteins synapsin I, GAP-43, and MAP-2 may play a role in the pathophysiology of depression and the mechanisms of antidepressants.
Analysis of Variance↗
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↗