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PubMed1999

Increased basal activity of the HPA axis and renin-angiotensin system in congenital learned helpless rats exposed to stress early in development.

Learned helpless behavior has been successfully bred in rats and designated as a genetic animal model of human depression and/or anxiety. Since congenital learned helpless animals have an impaired stress response in adulthood, we examined the effects of early stressors (at postnatal day 7, 14 or 21) on the hypothalamic-pituitary-adrenal axis and the renin-angiotensin system. The functioning of the hypothalamic-pituitary-adrenal axis was monitored through changes in corticosterone plasma levels in the adult animals after acute exposure to cold stress and maternal deprivation early in development. Renin-angiotensin system functioning was assessed by plasma renin activity. Unstressed congenital learned helpless rats had corticosterone levels that were similar to control animals (congenital non-learned helpless rats not stressed during development), but unstressed plasma renin activity levels of congenital learned helpless rats were lower than congenital non-learned helpless rats. There was a step-wise increase in corticosterone plasma levels in the congenital learned helpless rats with age of acute presentation of either cold stress or maternal deprivation stress (day 7, 49%; day 14, 84%; and day 21, 543% for cold stress). However, these baseline corticosterone levels were significantly lower in congenital learned helpless rats compared to congenital non-learned helpless controls. Similarly, in response to early exposure to cold stress and maternal deprivation, there was an increase in plasma renin activity levels of congenital learned helpless rats with age of presentation to either stressors. However, this increase in plasma renin activity levels was not evident in congenital non-learned helpless controls. Taken together, these results suggest that exposure to stress early in development has long-term effects on both the hypothalamic pituitary-adrenal axis and the renin-angiotensin system, two neuroendocrine indicators of stress responsivity.

Animals↗
PubMed1990

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↗
PubMed1999

Decrease in stress-induced c-Fos-like immunoreactivity in the lateral septal nucleus of learned helpless rats.

Inescapable stress can induce learned helplessness in many species of animals. Learned helplessness is a phenomenon which has some behavioral and neurotransmitter analogies with human clinical depression. Stress can also induce the expression of immediate early genes, including c-fos in many areas of the central nervous system. We examined stress-induced c-Fos-like immunoreactivity (FLI) using the learned helplessness paradigm. Naive rats showed significantly higher FLI than the tested groups in all the amygdaloid regions and in the hypothalamic paraventricular nucleus. However, in the lateral septal nucleus, helpless animals showed significantly reduced FLI in response to stress, compared to the other groups. These, and other previous data, highlight the importance of the septal area in mediating behavioral responses to inescapable stress.

Animals↗
PubMed1997

Lack of shuttlebox avoidance learning in autoimmune BXSB mice: a test of learned helplessness.

1. The authors investigated whether learned helplessness was a possible explanation for the observed learning deficits demonstrated by autoimmune mice in shuttlebox avoidance. If mice were experiencing learned helplessness during the avoidance testing, one would expect this to transfer to other behavioral tests resulting in lower learning scores. 2. One group of BXSB mice was tested in avoidance first, a water version of the Lashley III maze second, and water escape last, while another group was given these tests in the reverse order. 3. Animals who were exposed to avoidance first did not demonstrate any learning deficits in subsequent tests, suggesting that there were no adverse effects of avoidance training on later water maze learning. 4. However, correlations between number of null responses during avoidance learning and two other measures suggest that the null response measure may be an index of a continuum of learned helplessness within the BXSB strain.

Animals↗
PubMed2004

Rats with congenital learned helplessness respond less to sucrose but show no deficits in activity or learning.

Inbred rat strains for congenital learned helplessness (cLH) and for congenital resistance to learned helplessness (cNLH) were investigated as a model to study genetic predisposition to major depression. Congenitally helpless rats respond less to sucrose under a progressive ratio schedule. This is not confounded by locomotor hypoactivity: in contrast, cLH rats show a slight hyperactivity during the first 5 min of an open field test. cLH rats acquire operant responding to sucrose as readily as cNLH rats and exhibit normal memory acquisition and retrieval in the Morris water maze, thus ruling out general learning deficits as the cause of the decreased response to sucrose. Reduced total responses and reduced breaking points for sucrose in the cLH strain argue for anhedonia, which is an analogue to loss of pleasure essential for the diagnosis of major depressive episodes, and thus confirm the validity of congenitally learned helpless rats as a model of major depression.

Animals↗
PubMed1988

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↗
PubMedDate not supplied

Treating learned helplessness in the elderly dementia patient: preliminary inquiry.

Learned helplessness is the psychological state that results when an individual who is unable to exercise reasonable mastery in one situation incorrectly assumes that he or she is then unable to exercise reasonable control in other situations as well. This may complicate the delivery of health interventions since the individual with learned helplessness may assume that no care provider or treatment intervention can be of assistance. Elderly patients with Alzheimer's disease and other dementias are not immune to this stance of learned helplessness. This paper presents one possible psychosocial rehabilitation approach, the Project SMART (Stress Management and Relaxation Training) program, to the problem of learned helplessness. Based on the skills of adaptive stress-resistant problem solvers, Project SMART can be adapted to the needs of the elderly demented. The clinical and research implications are discussed.

Aged↗
PubMed1993

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↗
PubMed2000

Gender differences in learned helplessness behavior are influenced by genetic background.

Learned helplessness behavior was examined in female and male C57BL/6J (B6), 129/J (129) and (B6 x 129)F1 mice, common genetic backgrounds for the generation of knockout models, as well as in mice of a mixed genetic background (outbred mice). Both genotype and gender differences were observed in learned helplessness. Outbred males showed increased shuttle escape latencies following 60, 120, or 360 inescapable shocks compared to nonshocked controls, but outbred females showed no increase in escape latencies following inescapable shock pretreatment. B6 females showed increased escape latencies following 60, 120, or 360 inescapable shocks, whereas B6 males showed increased latencies only after 360 shocks. Female and male 129 and B6129F1 mice did not show an increase in escape latencies following inescapable shock, but this was most likely due to poor escape performance in nonshocked control mice. Differences in escape performance could not be explained by differences in pain thresholds between genotypes. These results support the idea that genetic background and gender are important to consider when using the learned helplessness model in genetically manipulated mice.

Animals↗
PubMed1989

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↗
PubMed1975

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↗
PubMed1982

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↗
PubMed1999

The Rheumatology Attitudes Index and its helplessness subscale are valid and reliable measures of learned helplessness in Asian patients with systemic lupus erythematosus.

OBJECTIVE: To assess the internal consistency, reliability, and construct validity of the Rheumatology Attitudes Index (RAI) and its subscales in a cohort of Asian patients with systemic lupus erythematosus (SLE). METHODS: English speaking ethnic Chinese, Malay, or Indian patients with SLE (n = 120) seen at a rheumatology unit completed a questionnaire containing the RAI twice within a 2 week period. Lupus activity was assessed using the British Isles Lupus Activity Group (BILAG) score, disease related damage using the Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) damage index, and quality of life using the Medical Outcome Survey Short Form 36 Health Survey (SF-36). Factor analysis and Cronbach's alpha were used to study the psychometric properties of the RAI. The magnitude of test-retest differences was assessed using the method of Bland and Altman. Relationships between the RAI, its helplessness (HS) and internality (IS) subscales, and BILAG, SLICC/ACR damage index and SF-36 scores were studied using Spearman's rank correlation. RESULTS: Factor analysis (n = 105) identified 2 factors corresponding to the HS and IS subscales of the RAI. All scales showed acceptable internal consistency, with Cronbach's alpha of 0.64 for the HS, 0.77 for the IS, and 0.74 for the RAI. Mean (SD) test-retest differences were 0.85 (3.96) points for the HS (n = 86), 0.81 (4.44) points for the IS (n = 85), and 1.46 (7.88) points for the RAI (n = 74). Six of 10 hypotheses relating the RAI and HS to demographic, disease, and quality of life variables were confirmed, supporting the construct validity of these scales. CONCLUSION: The RAI and its helplessness subscale are valid and reliable measures of learned helplessness in a multiethnic cohort of Asian patients with SLE in Singapore.

Adolescent↗
PubMed1983

[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↗
PubMedDate not supplied

Beta-adrenergic receptor changes in learned helplessness may depend on stress and test parameters.

Behavioral deficits following inescapable stress (learned helplessness) may serve as an animal model of depression. Previous studies using foot-shock stress to induce learned helplessness and a bar-press test for the stress-induced behavioral deficit have found increased beta-adrenergic receptor density in the hippocampus of learned helpless rats. We replicated these experiments using a tail-shock stress and the shuttle-box test. In our experiments, rats that developed learned helplessness after inescapable stress did not demonstrate any significant differences in beta-adrenergic receptor density or affinity in the frontal cortex, cerebellum, or hippocampus compared to the nonhelpless rats, nor to the tested control rats. These results suggest that beta-adrenergic receptor changes in learned helplessness may depend on the specific stress and test procedures used.

Animals↗
PubMed2000

Hypertension and insulin resistant models have divergent propensities to learned helpless behavior in rodents.

The induction of learned helpless (LH) behavior in rats is a widely used model of unipolar depression. Recent studies have linked depression with hypertension and insulin resistance as observed in obesity, but the propensity of these disorders to manifest depression has not been reported. In this study, the LH behavioral paradigm was exploited in a model of hypertension (Dahl rat) and of insulin resistance (Zucker rat) to determine the propensity of these models to develop depression and to examine the profile of markers for the propensity of the cardiovascular system (plasma renin activity) and of the hypothalamus-pituitary-adrenal axis (corticosterone) in the display of propensity to depression. Results show that Zucker rats displayed the lowest propensity to the development of LH behavior (12%), followed by the control Sprague-Dawley rats (27%), and then Dahl rats (66%). In contrast, congenital learned helpless (cLH) rats, a genetically bred strain for animal depression, had the highest propensity (>90%). A gender effect was observed in the Zucker and cLH rats, with females showing an increased propensity to develop LH behavior. Plasma renin activity in the Dahl and Sprague-Dawley rats after the LH stress paradigm was not significantly different from baseline. In contrast, Zucker rats, with the lowest propensity to LH behavior, demonstrated a threefold increase in plasma renin activity after stress. Congenital LH rats, with the highest propensity to LH behavior, exhibited a significantly lower increase (43%) in plasma renin activity after stress. Hyporesponsive hypothalamus-pituitary-adrenal (HPA) axis functioning correlated with propensity of LH behavior. Stress-induced corticosterone levels increased under twofold in cLH rats, whereas they increased more than sevenfold in Zucker rats. Taken together, these studies suggest that whereas genetically prone hypertensive rats have a very high propensity to depression, insulin-resistant rats have a profound resistance to depression. Moreover, a hyporesponsive HPA axis may be a marker for disorders that are comorbid with depression, whereas a hyperresponsive renin-angiotensin system may be indicative of resilience.

Animals↗
PubMed1986

Attributional processes in the learned helplessness paradigm: behavioral effects of global attributions.

Following the learned helplessness paradigm, I assessed in this study the effects of global and specific attributions for failure on the generalization of performance deficits in a dissimilar situation. Helplessness training consisted of experience with noncontingent failures on four cognitive discrimination problems attributed to either global or specific causes. Experiment 1 found that performance in a dissimilar situation was impaired following exposure to globally attributed failure. Experiment 2 examined the behavioral effects of the interaction between stable and global attributions of failure. Exposure to unsolvable problems resulted in reduced performance in a dissimilar situation only when failure was attributed to global and stable causes. Finally, Experiment 3 found that learned helplessness deficits were a product of the interaction of global and internal attribution. Performance deficits following unsolvable problems were recorded when failure was attributed to global and internal causes. Results were discussed in terms of the reformulated learned helplessness model.

Adult↗