Three accounts of the learned helplessness effect

Two experiments tested predictions drawn from test anxiety theory, learned helplessness theory, and Wortman and Brehm's (1975) integration of helplessness and reactance theories. Experiment 1 demonstrated that performance deficits predicted by learned helplessness do not rely on experimenter-induced failure. It also showed such deficits to be unrelated either to negative affect following exposure to pretreatment or to causal attributions about pretreatment task performance. Experiment 2 showed that experience of uncontrollability need not result in impaired performance, because failure on an unimportant task did not produce the deficits predicted by learned helplessness theory. This result provides qualified support for the integrative model. Finally, because the subjective measures used in Experiment 2 were not consistent with performance measures, the reliability of self-reports is questioned.     

Learned helplessness as conditioned inattention to the target stimulus

Learned helplessness theory explains the impaired performance that follows exposure to uncontrollable outcomes by assuming learned expectation of response-outcome independence that is transferred between tasks. Recent evidence has shown that introducing a second neutral stimulus, contingent on the offset of the uncontrollable stimulus, removes the subsequent interference. This finding has been claimed to support the view that the interference is a result of conditioned inattention rather than of the expectation of response-outcome independence. These conflicting explanations were examined in a series of four experiments that varied induction procedures (passive exposure or inescapability) and stimulus quality (aversive or nonaversive). All four experiments found the predicted interference, but only one, in which passive exposure was combined with an aversive stimulus, obtained results supporting the conditioned inattention hypothesis. We conclude that learned helplessness probably involves more than a single mechanism and that the passive exposure procedure may not be appropriate for demonstrating genuine helplessness deficits.     

Stress, Glucocorticoids, and Damage to the Nervous System: The Current State of Confusion

An extensive literature demonstrates that glucocorticoids (GCs), the adrenal steroids secreted during stress, can have a broad range of deleterious effects in the brain. The actions occur predominately, but not exclusively, in the hippocampus, a structure rich in corticosteroid receptors and particularly sensitive to GCs. The first half of this review considers three types of GC effects: a) GC-induced atrophy, in which a few weeks' exposure to high GC concentrations or to stress causes reversible atrophy of dendritic processes in the hippocampus; b) GC neurotoxicity where, over the course of months, GC exposure kills hippocampal neurons; c) GC neuroendangerment, in which elevated GC concentrations at the time of a neurological insult such as a stroke or seizure impairs the ability of neurons to survive the insult. The second half considers the rather confusing literature as to the possible mechanisms underlying these deleterious GC actions. Five broad themes are discerned: a) that GCs induce a metabolic vulnerability in neurons due to inhibition of glucose uptake; b) that GCs exacerbate various steps in a damaging cascade of glutamate excess, calcium mobilization and oxygen radical generation. In a review a number of years ago, I concluded that these two components accounted for the deleterious GC effects. Specifically, the energetic vulnerability induced by GCs left neurons metabolically compromised, and less able to carry out the costly task of containing glutamate, calcium and oxygen radicals. More recent work has shown this conclusion to be simplistic, and GC actions are shown to probably involve at least three additional components: c) that GCs impair a variety of neuronal defenses against neurologic insults; d) that GCs disrupt the mobilization of neurotrophins; e) that GCs have a variety of electrophysiological effects which can damage neurons. The relevance of each of those mechanisms to GC-induced atrophy, neurotoxicity and neuroendangerment is considered, as are the likely interactions among them.     

Peripheral vision monitor: Presenting displays at known positions in the visual periphery

The peripheral vision monitor is an inexpensive device that ensures that visual stimuli can be successfully projected to a given extrafoveal location. The apparatus extinguishes the display lighting system when the observer attempts to view a region intended to be viewed only in peripheral vision, reinstating the illumination when that region is again in the peripheral field. This is achieved by focusing a small spot of light on the scleral-corneal boundary of the observer’s eye and detecting the reflected light with a photocell and circuit. Illumination changes produced at the photocell are used to trigger the display lighting.     

Women's Dress Fashions as a Function of Reproductive Strategy

Despite many speculations, there is no well-supported explanation for cycles of fashion in.women's dress and scholars cannot agree whether fashions reflect societal changes. Generalizing from cycles of bodily attractiveness for women, it was hypothesized that dress styles are reflective of reproductive economics. Using data from three studies of dress fashion extending from 1885-1976, the prediction was tested thatshortskirts (signaling sexual accessibility) would be correlated with low sex ratios (indicating limited marital opportunity for women), with increased economic opportunities for women and with marital instability. Predictions for narrowwaists and low necklines (which signal reproductive value) were opposite. These predictions received strong support indicating that dress styles, like standards of bodily attractiveness may be partly determined by marital economics.     

Lesions of the intermediate medial hyperstriatum ventrale impair sickness-conditioned learning in day-old chicks.

Lesion studies show that the intermediate medial hyperstriatum ventrale (IMHV), a forebrain visual association area in chicks, is involved in learning and memory for one-trial passive avoidance and imprinting. We examined the effects of IMHV lesions in a one-trial, nongustatory, sickness-conditioned learning task. This task is similar to passive avoidance and imprinting because all three tasks require the chick to remember visual cues in order to respond correctly. However, sickness-conditioned learning differs from imprinting and passive avoidance because it uses sickness as the aversive stimulus and there is a longer conditioned stimulus-unconditioned stimulus interval (30-min delay compared to seconds). Bilateral IMHV lesions given 24 h before training impaired the ability of the chicks to avoid a bead associated with sickness produced by lithium chloride injection, as did pretraining unilateral left or right IMHV lesions. Post-training IMHV lesions given 1 h after training did not impair avoidance of the test bead in the sickness-conditioned learning task. However, lesioned chicks showed generalized avoidance of all test beads. The pretraining lesion results are similar to those found in imprinting and passive avoidance learning; however, the effects of unilateral IMHV lesions differed. Post-training lesion effects are similar to those found in passive avoidance learning. We propose that both left and right IMHV are necessary for sickness-conditioned learning and that post-training IMHV lesions impair the ability of the chick to learn or remember the association between the color of the bead and the aversive consequences of LiCl injection.