The Wistar Hannover rat (WHR) is a strain commonly used for toxicity studies but rarely used in studies investigating depression neurobiology. In this study, we aimed to characterise the behavioural responses of WHR to acute and repeated antidepressant treatments upon exposure to the forced swim test (FST) or learned helplessness (LH) test. WHR were subjected to forced swimming pre-test and test with antidepressant administration (imipramine, fluoxetine, or escitalopram) at 0, 5 h and 23 h after pre-test. WHR displayed high immobility in the test compared to unstressed controls (no pre-swim) and failed to respond to the antidepressants tested. The effect of acute and repeated treatment (imipramine, fluoxetine, escitalopram or s-ketamine) was then tested in animals not previously exposed to pre-test. Only imipramine (20 mg/kg, 7 days) and s-ketamine (acute) reduced the immobility time in the test. To further investigate the possibility that the WHR were less responsive to selective serotonin reuptake inhibitors, the effect of repeated treatment with fluoxetine (20 mg/kg, 7 days) was investigated in the LH model. The results demonstrated that fluoxetine failed to reduce the number of escape failures in two different protocols. These data suggest that the WHR do not respond to the conventional antidepressant treatment in the FST or the LH. Only s-ketamine and repeated imipramine were effective in WHR in a modified FST protocol. Altogether, these results indicate that WHR may be an interesting tool to investigate the mechanisms associated with the resistance to antidepressant drugs and identify more effective treatments.

The current study assessed whether the proportion of childhood (age 0–9 years) in poverty altered the developmental trajectories (ages 9–24) of multimethodological indicators of psychological well-being. In addition, we tested whether exposure to cumulative risk over time mediated the association between poverty exposure and psychological well-being. Measures of psychological well-being included internalizing and externalizing symptoms, a behavioral index of learned helplessness (task persistence), and chronic physiological stress (allostatic load). Exposure to poverty during childhood predicted the trajectory of each development outcome: individuals with more poverty exposure during childhood showed (a) relatively high levels of internalizing symptoms that diminished more slowly with maturation, (b) relatively high levels of externalizing symptoms that increased faster over time, (c) less task persistence indicative of greater learned helplessness, and (d) higher levels of chronic physiological stress which increased faster over time relative to persons with less childhood poverty exposure. Trajectories of cumulative risk exposure from physical and psychosocial surroundings from 9–24 years accounted for the association between childhood poverty and the growth curves of internalizing and externalizing symptoms but not for learned helplessness or chronic physiological stress. Additional sensitivity analyses indicate that early childhood disadvantage is particularly problematic for each outcome, except for internalizing symptoms which seem sensitive to the combination of early and lifetime poverty exposure. We also explored whether domains of cumulative risk as well as two alternatives, maternal sensitivity or family cohesion, functioned as mediators. Little evidence emerged for any of these alternative mediating constructs.

In this article, we evaluate gender differences in COVID-19 conspiracy theory beliefs. We find that women are significantly less likely than men to endorse COVID-19 conspiracy theories and that this gender difference cuts across party lines. Our analysis suggests that this gender gap is partially explained by two dispositional factors: learned helplessness and conspiratorial thinking. Our findings qualify past work on the antecedents of conspiracy theory beliefs, which does not uncover robust and significant gender differences. The results highlight the need for work in this area to better theorize about the significance of gender.

The influence of an adrenal medullary transplant into the lumbar subarachnoid space on learned helplessness, an animal model of depression, was examined. The transplanted rats were found to be less susceptible than sham-operated animals to become helpless after administration of inescapable shocks. The effect was attributed to release of opioid peptides by chromaffin cells as it was reversed by naloxone. The viability of the transplanted tissue was verified by electron microscopy.

The article retraces the shifting conceptualizations of psychological trauma in experimental psychopathological research in the middle decades of the twentieth century in the United States. Among researchers studying so-called experimental neuroses in animal laboratories, trauma was an often-invoked category used to denote the clash of conflicting forces believed to lead to neurotic suffering. Experimental psychologists, however, soon grew skeptical of the traumatogenic model and ultimately came to reject neurosis as a disease entity. Both theoretical differences and practical circumstances, such as the technical challenge of stabilizing neurotic symptoms in rats, led to this demise. Yet, despite their reservations, experimental psychologists continued to employ traumatic stimuli to produce psychopathological syndromes. In the 1960s, a new understanding of trauma evolved, which emphasized the loss of control experienced by traumatized animal subjects. These shifting ideas about trauma, I argue, reflect both varying experimental cultures, epistemic norms as well as changing societal concerns.

An hypothesis based on the original stress model of depression, learned helplessness, proposed that exposure to uncontrollable stress provides the basis, in animals as in humans, for learning that stress is uncontrollable (helplessness); this learning has a number of debilitating consequences, including depression. This study suggests that rats subjected to daily restraint sessions (1h × 5 d, in 20 × 10 × 10 cm boxes) displayed a quiescent behavior vvith few attempts to escape from the box during the restraint periods, and subsequently exhibited escape deficits in a shuttle-box. These deficits were eliminated by clomipramine (8 or 16 mg/kg), imipramine (16 mg/kg) and nialamide (16 mg/kg) given twice daily subsequent to the last restraint session. In contrast, diazepam (2 mg/kg/d) or sulpiride (8 mg/kg/d) did not reduce helpless behavior induced by daily restraint sessions. In addition reduction in locomotor activity has been reported in rats subjected to restraint. It is suggested that the experience of loss of control thought to result from unsuccessful attempts to escape the stressor could be the critical aspect of behavior sensitive to antidepressants.