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PubMed1982

Cognitive influences on the development of learned helplessness.

College students (N = 120) participated in experiment concerning the influence of self-statements following failure on subsequent symptoms of learned helplessness. One third of the students were given solvable concept-formation problems (nonhelpless condition) and two thirds were given unsolvable concept-formation problems (helpless condition). A multivariate analysis of variance revealed a significant difference between helpless and nonhelpless students on cognitive/motivational and affective measures of learned helplessness and on self-statements regarding performance. However, when multiple regression and correlational analyses were performed within the group of students who failed the concept-formation problems, no stable relationship was found between self-statements (cognitions) about concept-formation performance and the measures of learned helplessness. The implications of these results for Beck's (1967) cognitive model of depression and the reformulated learned helplessness model of depression (Abramson, Seligman, & Teasdale, 1978) are discussed.

Cognition↗

PubMed1992

Prevention of learned helplessness: in vivo correlation with cortical serotonin.

Learned helplessness (LH) is prevented by pretreatment with acute benzodiazepines (BDZs), subchronic tricyclic antidepressants (TCAs), or escapable stress (ES). We have investigated the role of serotonin (5-HT) in LH prevention by these three prevention paradigms, using microdialysis to measure in vivo 5-HT release in frontal cortex (FC) after LH testing. Rats receiving pretreatment before inescapable stress with any of the three methods of prevention--BDZs, TCAs, or ES--showed escape behavior in the shuttle-box test for LH comparable to naive unstressed controls. K(+)-stimulated 5-HT release in all three groups receiving pretreatment was also similar to naive unstressed controls. Rats receiving saline before inescapable stress showed significantly more LH behavior in the shuttle-box task and had significantly lower 5-HT release as well. This suggests that LH correlates with a significant decrease in intracellular releasable 5-HT in FC, and that three different techniques for LH prevention, acute BDZs, subchronic TCAs, and ES all similarly prevent this 5-HT depletion.

Animals↗

PubMed1994

Does learned helplessness induction by haloperidol involve serotonin mediation?

Learned helplessness (LH) is a behavioral depression following inescapable stress. Helpless behavior was induced in naive rats by the dopamine D2 receptor blocker haloperidol (HDL) in a dose-dependent manner, with the greatest effects seen at 20 mg/kg (IP). Rats were tested 24 h after injection. Haloperidol (IP) increased release of serotonin (5-HT) in medial prefrontal cortex (MPC) as measured by in vivo microdialysis. Perfusion of HDL through the probe in MPC caused increased cortical 5-HT release, as did perfusion of both dopamine and the dopamine agonist apomorphine. Our previous work found that increased 5-HT release in MPC correlates with the development of LH. The present work suggests that increased DA release in MPC, known to occur with both inescapable stress and with HDL, may play a necessary but not sufficient role in the development of LH. Also, this suggests that increased DA activity in MPC leads to increased 5-HT release in MPC and to subsequent behavioral depression.

Animals↗

PubMed1985

The distortion of self-perception by learned helplessness.

This study examined the impact of learned helplessness on self-perception of competence. The participants were 180 undergraduates who were placed in control, failure, or success groups where they were given a list of traits on which to evaluate themselves, followed by an anagram-solution test. Significant performance effects were observed on the test; self-assessment was more representative of actual ability, however, than of the treatment situation. The results suggest that although experiencing uncontrollable failure may result in performance deficits, perception of ability may not be distorted.

Achievement↗

PubMed2003

High- and low-structure treatments for substance dependence: role of learned helplessness.

We studied whether pretreatment levels of learned helplessness (LH) were related to outcomes for substance-dependent individuals receiving high-structure, behaviorally oriented (HSB) or low-structure, facilitative (LSF) treatment. The subjects were 120 substance-dependent patients randomly assigned to the HSB or the LSF treatment style for up to 12 weeks of weekly individual counseling. The two groups were compared across pretreatment characteristics as well as in-treatment, end-of- treatment, and 9-month postadmission follow-up outcome measures. Outcomes reflected reduction in problem severity, abstinence, retention, dropout rate, and ratings of treatment benefit. Significant and comparable reductions in symptoms occurred for the HSB and LSF patients both during treatment and at follow-up. Comparisons of other outcomes also did not consistently favor either treatment style. However, significant and consistent interactions were observed between LH and treatment styles with respect to several outcome measures, and these effects were independent of pretreatment levels of depression, addiction severity, and readiness for treatment. Specifically, the more "helpless" patients did significantly better in HSB treatment, whereas the less "helpless" patients had better outcomes in LSF treatment. A matching approach that assigns patients to high- and low-structure treatments based on pretreatment levels of LH might improve treatment outcomes for substance-dependent patients.

Analysis of Variance↗

PubMed1997

Effects of naltrexone and cross-tolerance to morphine in a learned helplessness paradigm.

Opiates have been implicated in learned helplessness (LH), a phenomenon known to be related to opiate stress-induced analgesia (SIA). In the present study, we investigated the role of opiates in the induction of LH and SIA under different conditions. Adult female Wistar rats were trained either by receiving 60 inescapable 1-mA footshocks (IS group, N = 114) or by confinement in the shock box (control or NS group, N = 92). The pain threshold of some of the animals was immediately evaluated in a tail-flick test while the rest were used 24 h later in a shuttle box experiment to examine their escape performance. The opiate antagonist naltrexone (0 or 8 mg/kg, ip) and the previous induction of cross-tolerance to morphine by the chronic administration of morphine (0 or 10 mg/kg, sc, for 13 days) were used to identify opiate involvement. Analysis of variance revealed that only animals in the IS group demonstrated antinociception and an escape deficit, both of which were resistant to the procedures applied before the training session. However, the escape deficit could be reversed if the treatments were given before the test session. We conclude that, under our conditions, induction of the LH deficit in escape performance is not opiate-mediated although its expression is opiate-modulated.

Analgesia↗

PubMed2003

Different regulation of adenylyl cyclase and rolipram-sensitive phosphodiesterase activity on the frontal cortex and hippocampus in learned helplessness rats.

The present study examined the activities of adenylyl cyclase (AC) and rolipram-sensitive phosphodiesterase (PDE4) on brain regions in learned helplessness rat in order to clarify the cyclic AMP (cAMP) regulation system in the depressive state. Rats exposed to inescapable footshocks once a day for 3 days exhibited a significant increase in escape failure on Day 1 (the day after the last inescapable shock day) and Day 7. The plasma corticosterone level in rats subjected to inescapable shocks was significantly higher than that of nonstressed control rats on Days 1 and 7. The PDE4 activity of the frontal cortex was significantly lower than that of nonstressed control rats on Day 1. However, on Day 7, the PDE4 and [3H]-rolipram binding activities were significantly increased in the frontal cortex and hippocampus of learned helplessness rats compared with those of nonstressed control rats. Forskolin-stimulated AC activity was significantly decreased in the frontal cortex, hippocampus and striatum of learned helplessness rats on Day 1, but not on Day 7. Thus, a decrease in both AC and PDE4 activities was noted in the acute depressive state. In contrast, increase of PDE4 activity was noted in the delayed depressive phase, although no change of AC activity was observed. Gel shift assays also showed the decrease of cAMP-response element (CRE)-binding activity relating to cAMP activity in the frontal cortex and hippocampus of learned helplessness rats on Days 1 and 7. These findings indicated a delayed increase in PDE4 activity leading to hypofunction of the cAMP-dependent signal transduction system in the frontal cortex and hippocampus of learned helplessness rats, suggesting that up-regulation of the cAMP-degradation system by PDE4 may play a pivotal role in pathological states of chronic depression.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1985

Depression and learned helplessness in mentally retarded and nonmentally retarded adolescents: an initial investigation.

Depression and learned helplessness were examined in a sample of 26 educably mentally retarded (EMR) adolescents and a matched (on age, sex, and race) group of 26 nonmentally retarded adolescents. Depression and learned helplessness were assessed using the Reynolds Adolescent Depression Scale (RADS) and Mastery Orientation Inventory (MOI), respectively. Results indicated that EMR adolescents manifested significantly (p less than .001) greater depressive symptomatology than their nonmentally retarded peers. Sex differences were also found, with females demonstrating greater depression scores in both groups. Analysis of severity of symptom endorsement showed significant group differences on items reflecting somatic, self-evaluative, and behavioral components of depression, with mentally retarded subjects demonstrating higher scores. Mentally retarded adolescents were found to score higher (p less than .001) on the learned helplessness measure than nonmentally retarded adolescents. Given the problematic nature of depression noted in large sample epidemiological studies of nonmentally retarded adolescents, the results of this investigation indicate that depression in EMR adolescents is an affective characteristic in need of further study.

Adolescent↗

PubMed1975

Frustation and learned helplessness.

This article reports the transfer of learned helplessness from one aversive motivator, shock to another, frustration. In experiment 1, animals were trained to approach food in a runway and concomitantly exposed to either escapable, inescapable, or no shock in a different situation. Extinction was conducted in the runway, and subsequently the animals were tested for hurdle-jump escape from the frustrating goal box. Inescapably shocked rats failed to learn to hurdle-jump, whereas escapably or nonshocked animals learned the frustration escape response. Experiment 2 replicated the basic finidngs of Experiment 1 and showed transfer of learned helplessness from shock to frustration when no running response had been first acquired in the runway.

Animals↗

PubMed1994

Using multiple risk factors to assess the behavioral, cognitive, and affective effects of learned helplessness.

Rather than examining the effect of the pessimistic explanatory style on an outcome variable reflecting a single domain, I studied the effects of multiple learned-helplessness risk factors on behavioral, cognitive, and affective variables. Undergraduate students completed the Learned Helplessness Scale (Quinless & McDermott-Nelson, 1988) as a measure of their expectation of uncontrollability and the Explanatory Style Questionnaire (Peterson et al., 1982) to determine their explanations for both positive and negative events. Results revealed a significant effect for risk level, with students at greater risk of helplessness reporting significantly more procrastination, lower grade point averages, and more dysphoria. These results support the use of multiple risk factors representing all learned-helplessness precursors and the assessment of learned-helplessness deficits drawn simultaneously from behavioral, cognitive, and affective domains.

Adult↗

PubMed1994

Learned helplessness sensitizes hippocampal norepinephrine to mild restress.

A proportion of rats exposed to inescapable tailshock stress displayed a performance deficit, termed learned helplessness, in a subsequent shuttlebox avoidance task. The technique of in vivo microdialysis was used to determine hippocampal norepinephrine levels in learned helpless, nonhelpless and nonprestressed control rats. Similar basal norepinephrine levels were detected in samples between rat groups. Following an exposure to a milder form of inescapable shock, an increase in norepinephrine output was detected in learned helpless rats, which was significantly greater than nonhelpless, nonprestressed, or control animals. Thus, inescapable stress appears to sensitize the hippocampus to increase norepinephrine release in response to a subsequent smaller stressor. This hypersensitivity might underlie the avoidance impairment of learned helplessness. Therefore, the possibility exists that similar neurochemical changes may also be responsible for some of the symptoms of human posttraumatic stress disorder (PTSD), such as the poor coping associated with seemingly mild stress.

Animals↗

PubMed1986

Attributional versus preattributional variables in self-esteem and depression: a comparison and test of learned helplessness theory.

Predictions made according to the attributional reformulation of learned helplessness theory concerning the cognitive determinants of low self-esteem and depression were tested in two samples of undergraduates; real and hypothetical life events were used. As predicted, internal attributions for hypothetical success and failure were correlated with self-esteem, but there was an unexpected correlation with global attributions for negative outcomes. Two "preattributional" variables, consensus and consistency judgments, were also related to self-esteem and depression. In contrast to learned helplessness theory, a path analysis indicated that these variables were not attributionally mediated. Consensus judgment was as strong a predictor of depression as the number of recent distressing life events that subjects had experienced. Other evidence that links depression to perceived low consensus is described, and a possible etiological role for this variable is outlined.

Adult↗

PubMed1993

Alterations in glucocorticoid inducible RNAs in the limbic system of learned helpless rats.

Glucocorticoids (GC) have an important effect on mood in humans and influence learned helplessness, an escape avoidance paradigm that is considered one of the best animal models of depression. A strong genetic component underlies the development of learned helplessness as shown by the emergence of a line of highly vulnerable rats (LH strain) through selective inbreeding. In addition, hormonal factors play a role. Adrenalectomy (adx) for example is known to increase the vulnerability to acquire learned helplessness, an effect that is reversed by glucocorticoids (GC). Since GC function primarily by modulating gene expression, hormone mediated alterations in mRNAs expressed in the brain may be important in the development of an adequate escape avoidance response. Conversely, we postulate that the deficit in escape avoidance behavior exhibited by the LH strain may be associated with an alteration in GC-mediated gene expression in the brain. To test this hypothesis, we analyzed GC-responsive mRNAs that are expressed in the hippocampus. Control Sprague-Dawley (SD) rats showed consistent alterations in mRNAs that are modulated by GC, such as type II GC receptor (GR) and metallothionein-1 (MT-1). Under our experimental conditions, both GR and MT-1 mRNA are significantly increased in the hippocampus of hormone-treated SD rats. An increase in hypothalamic GR mRNA was also observed. However, under the same experimental conditions, LH rats showed more selective hormone induced changes since GC had no effect on hypothalamic and hippocampal GR mRNA whereas a significant increase in MT-1 mRNA was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗

PubMed2003

Reduced cell proliferation in the dentate gyrus is not correlated with the development of learned helplessness.

BACKGROUND: A plethora of indirect findings suggests that mood disorders may be caused by or result in structural changes in the brain, namely decreased hippocampal cell proliferation. METHODS: To test for these hypotheses, we used a rat model of depression, learned helplessness. Moderate unpredictable and inescapable foot shocks induced learned helplessness only in a portion of the rats. Rats that showed helpless behavior were compared to those behaving normally after inescapable shock. Proliferating cells in the dentate gyrus were labeled with BrdU (bromodeoxyuridine). RESULTS: Helpless behavior appeared before the decrease of dentate gyrus cell proliferation was maximal. Cell proliferation was decreased to the same extent in animals that developed helplessness as those that were not helpless. Furthermore, immobilization stress, which reduced the rate of cell proliferation, did not induce learned helplessness. CONCLUSION: These results are in line with reports that the rate of dentate gyrus cell proliferation is acutely down-regulated by stress, but the development of helpless behavior does not correlate with this process. Further studies will have to clarify if during learned helpless behavior neurogenesis is impaired by altered differentiation or survival of cells.

Analysis of Variance↗

PubMed2000

Antidepressant-like effects of the subtype-selective nicotinic acetylcholine receptor agonist, SIB-1508Y, in the learned helplessness rat model of depression.

RATIONALE: Epidemiological studies of smokers suggest that there is a link between nicotine and depression. Nonetheless, few studies have examined the potential use of nicotinic ligands in the treatment of depression. OBJECTIVES: The goal of this study was to evaluate the effects of SIB-1508Y, a novel subtype-selective ligand for high affinity nicotinic acetylcholine receptors (nAChRs), in the learned helplessness model of depression in rats. METHODS: In this model, exposure to inescapable foot-shock produces a lasting deficit in escape responses emitted in a subsequent conditioned avoidance procedure (learned helplessness). The effect of SIB-1508Y on learned helplessness was compared to the clinically used antidepressants, imipramine and fluoxetine, and the non-selective nAChR ligand, nicotine. RESULTS: Similarly to imipramine and fluoxetine, subchronic treatment (5 days) with SIB-1508Y reversed the escape deficit in the learned helplessness model in a dose dependent manner. The effect of SIB-1508Y on learned helplessness was still apparent 1 week following drug administration and was also maintained after 4 weeks of daily administration. In contrast, while nicotine was able to attenuate the learned helplessness deficit, this trend only reached statistical significance after chronic administration. The non-competitive ion channel blocker mecamylamine increased escape failures when administered alone and blocked the effects of SIB-1508Y but not imipramine. SIB- 1508Y also produced an increase in avoidance responding, which suggests an enhancement of learning. CONCLUSION: These results not only suggest a role for nAChRs in the development of a depressive-like syndrome, but also that subtype-selective nAChR agonists, such as SIB-1508Y, may offer a novel therapeutic approach to the treatment of depression.

Animals↗

PubMed2003

Specific creatine rise in learned helplessness induced by electroconvulsive shock treatment.

Metabolic changes in the hippocampus formation can be investigated with in vivo magnetic resonance spectroscopy (MRS). Learned helplessness (LH) is a well validated animal model of depression which we established in Sprague-Dawley rats defining some as "learned helpless" (LH) or not "learned helpless" (NLH). Helpless and non-helpless rats received a course of daily administered electroconvulsive shocks (ECS) for 6 days. MRS measurements were performed on a 4.7 T animal scanner with an average voxel size within the rat hippocampus of 10 microl. In LH rats hippocampal creatine/NAA rose significantly (14%) whereas creatine/NAA of NLH rats showed no increase at all. A possible connection between hippocampal creatine levels and major depressive disorders as a reflection of changes in energy metabolism is discussed.

Animals↗

PubMed2001

Mechanism of action of flibanserin in the learned helplessness paradigm in rats.

The mechanism of action of flibanserin, a 5-HT(1A) receptor agonist and a 5-HT(2A) receptor antagonist, was investigated in learned helplessness in rats. The effect of flibanserin (32 mg/kg, i.p. 30 min before testing) on learned helplessness was not antagonized by the (a) 5-HT synthesis inhibitor parachlorophenylalanine (pCPA; 150 mg/kg p.o.x3 times), which reduced brain 5-HT by 89%; (b) 5-HT(1A) receptor antagonists (+/-)-N-tert-butyl-3-4-(2-ethoxyphenyl)piperazin-1yl-2-phenyl propionamide [WAY100135; 10 mg/kg, i.p. 30 min before flibanserin, or 40 mg/kg, s.c. 15 min before flibanserin] and tertatolol (2.5 and 5 mg/kg, i.p. 30 min before flibanserin); and (c) 5-HT(2) receptor agonist (+/-)-2,5-dimethoxy-4-iodoamphetamine (DOI; 3 mg/kg, s.c. simultaneously with flibanserin). The effect of flibanserin on learned helplessness was antagonized by the dopamine D(1) receptor antagonist [R]-3-methyl-7-chloro-8-hydroxy-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine (SCH 23390; 0.1 mg/kg, i.p. 30 min before flibanserin) and by the opioid receptor antagonist naloxone (3 mg/kg, s.c. 15 min before flibanserin). Flibanserin (32 and 64 mg/kg) did not induce conditioned place preference. In conclusion, flibanserin improved rats' performance in the learned helplessness paradigm, by stimulating dopamine D1 and opioid receptors, probably indirectly, since flibanserin has a low affinity for these receptors.

Animals↗

PubMed1996

Learned helplessness, attributional style, and depression in epilepsy. Bozeman Epilepsy Surgery Consortium.

PURPOSE: We wished to examine the relevance of the theory of learned helplessness in general, and attributional style in particular, to the understanding of depression among patients with epilepsy. METHODS: Patients with lateralized temporal lobe epilepsy (TLE) (right = 73, left = 70) were administered two self-report depression inventories [Beck Depression Inventory (BDI), Center for Epidemiological Studies-Depression scale (CES-D)]. Depression scores were examined in relation to a key component of the revised theory of learned helplessness (attributional style) using the Optimism/Pessimism Scale. RESULTS: Attributional style was significantly associated with increased self-reported depression and remained significant when the effects of several confounding variables were controlled [age, age at onset, laterality of TLE, sex, and method variance]. CONCLUSIONS: The results indicate that the concept of learned helplessness in general, and attributional style in particular, are related to the genesis of depression in epilepsy. Because they are known to be related to depression in the general population, and because specific techniques for intervention and prevention are available, greater consideration of learned helplessness and attributional style in the genesis of depression in epilepsy may be worthwhile.

Adult↗