Raymond L. Jackson

Learned helplessness, inactivity, and associative deficits: effects of inescapable shock on response choice escape learning.

These experiments explored whether exposure to inescapable shock produces a subsequent deficit in the organisms propensity to associate its behavior with shock termination. Previous experiments are incapable of resolving this question because they confound reduced associability and decreased activity. Four experiments examined the effects of inescapable shock on the acquisition of Y-maze escape. Here, escape is accomplished by choosing the correct response from two available alternatives rather than by simple locomotion as in a shuttle box. By itself, reduced activity should not produce inaccurate choices, only slow choices. Experiment 1 found that inescapable shock produced slow learning of the correct choice for escape, even though active choices occurred on every trial. Further, the speed and accuracy of choice were not correlated. The second experiment showed that the choice escape learning deficit was produced by the inescapability of the shocks. Experiment 3 demonstrated that the choice accuracy of inescapably shocked rats was not improved by increases in Y-maze shock intensity, even though speed of responding was increased. The final experiment revealed that the effects of inescapable shock on Y-maze acquisition did not dissipate across a 1-wk period.

Learned Helplessness: All of us were Right (And Wrong): Inescapable Shock has Multiple Effects

Publisher Summary Organisms exposed to inescapable and unavoidable aversive events show later deficits in learning to escape such events when escape is possible This phenomenon, which has been called the “learned helplessness effect” and the “interference effect,” has received a great deal of recent attention and many of its characteristics are now known. This chapter explores the causes and explanations of this phenomenon, rather than all of its empirical characteristics, and present new evidence bearing on these issues. It also discusses inactivity hypotheses and examines that inescapable shock exposure induces reduced activity in the presence of shock. A discussion is presented on the research and theorizing directed at uncovering the mechanisms which produce the basic learned helplessness effect. The focus is on what exposure to inescapable aversive events does to the organism so that it later performs poorly in escape learning tasks. The implications of the work on learned helplessness for the psychology of learning in general is explored. The data presented in the chapter makes it clear that the existence of an activity deficit does not mean that the mechanisms that make up the learned helplessness hypothesis do not exist.

Exposure to inescapable shock produces both activity and associative deficits in the rat

Abstract Interference with shuttle-box escape learning following exposure to inescapable shock is often difficult to obtain in rats. The first experiment investigated the role of shock intensity during escape training in the apparent fragility of the effect. Experiment 1A demonstrated that the magnitude of the interference effect was systematically related to shock intensity during shuttle-box testing. At .6 mA, a robust effect was obtained, whereas at .8 mA and 1.0, little or no deficit in the escape performance of inescapably shocked rats was observed. Experiment 1B demonstrated that the deficit observed in Experiment 1A depended upon whether or not rats could control shock offset. Experiment 2 suggested that preshock may suppress activity and that higher shock levels may overcome this deficit. Experiment 3 tested this as the sole cause of the escape deficit by requiring an escape response which exceeded the level of activity readily elicited by a 1.0-mA shock in both restrained and preshocked rats. In such a task, preshocked rats performed more poorly than did restrained controls. These results are consistent with the possibility that inescapable shock may, in addition to reducing activity, produce an associative deficit. Experiment 4 more clearly demonstrated that inescapable shock produces deficits in performance which cannot be expleined by activity deficits and which appear to be associative in nature. It was shown that inescapable shock interfered with the acquisition of signaled punishment suppression but not CER suppression. The theoretical implications of these data for explanations of the manner in which prior exposure to inescapable shock interferes with escape learning were discussed.

Effects of task-irrelevant cues and reinforcement delay on choice-escape learning following inescapable shock: evidence for a deficit in selective attention.

Prior exposure to inescapable shock has been reported to interfere with choice-escape learning, but several investigators have failed to obtain this effect. A series of five experiments examined the conditions under which choice-escape learning in an automated Y-maze is impaired by pretreatment with inescapable shock. Inescapably shocked rats made more errors and responded more slowly than did controls only when shock termination was delayed and task-irrelevant cues were present during choice-escape training. These findings are discussed in terms of information processing and neurochemical consequences of exposure to inescapable shock.

Conditioned analgesia in the rat

It has been suggested by recent studies that the analgesic reaction to electric shock can be conditioned. However, these studies either lacked shocked controls or used an indirect measure of analgesia (freezing). In the present investigation, each rat was exposed an equal number of times to two distinct environmental contexts. The rats were shocked in one context and reexposed to the same context before test, shocked in one context and reexposed to the nonshock context before test, or not shocked at all and reexposed to one of the two contexts. Immediately following reexposure, the pain reactivity of the rats was assessed by a hot plate (Experiment 1) and a tail-flick apparatus (Experiment 2). It was found that rats that were reexposed to the context in which they had been shocked were significantly more analgesic than rats in the other two groups (which did not differ). These results confirm that it is possible to condition shock-induced analgesia in the rat.

The time course of learned helplessness, inactivity, and nociceptive deficits in rats

Abstract Four experiments are reported which explore the nature of the effects of inescapable shock on subsequent shuttlebox escape learning. The first experiment demonstrated that shuttle escape deficits dissipate within 48 hr after treatment with inescapable shock. Experiment 2 showed that exposure to inescapable shock suppressed unlearned activity in the shuttlebox and that this activity deficit recovered within 48 hr. Experiment 2A demonstrated that this shuttlebox crossing decrement was at least partly attributable to the inescapability of the shocks. These results suggested that activity factors might partly mediate the shuttle escape learning deficit reported in Experiment 1. Experiment 3 explored the possibility that activity and shuttle escape learning deficits are subserved by the effects of inescapable shock on pain sensitivity. The results supported this notion. It was found that rats were less sensitive to painful stimulation 24 hr after inescapable shock and that this analgesic tendency also dissipated within 48 hr after pretreatment. The implications of these results were discussed.

Retardation of autoshaping following pretraining with unpredictable food: Effects of changing the context between pretraining and testing ☆

Abstract In Experiment 1, pigeons exposed to US ONLY pretraining were observed to be retarded in the acquisition of autoshaping relative to naive controls; however, gross changes in contextual stimuli between pretraining and testing alleviated the retardation effect. In Experiment 2, groups of pigeons exposed to CS ONLY, US ONLY, or random CS-US presentations (TRC) were tested for the acquisition of autoshaping. The US ONLY and TRC groups were retarded relative to naive controls. The context change manipulation eliminated the US ONLY retardation effect and attenuated, but did not eliminate, the TRC retardation effect. Context blocking accounts for the US ONLY effect and contributes to the TRC effect; however, context-independent retardation following TRC pretraining suggests the operation of the learned irrelevance cognition.

Effects of Signaling Inescapable Shock on Subsequent Escape Learning: Implications for Theories of Coping and "Learned Helplessness"

The present experiments reveal that shuttle-escape performance deficits are eliminated when exteroceptive cues are paired with inescapable shock. Experiment 1 indicated that, as in instrumental control, a signal following inescapable shock eliminated later escape performance deficits. Subsequent experiments revealed that both forward and backward pairings between signals and inescapable shock attenuated performance deficits. However, the data also suggest that the impact of these temporal relations may be modulated by qualitative aspects of the cues because the effects of these relations depended upon whether an increase or decrease in illumination (Experiment 2) or a compound auditory cue (Experiment 4) was used. Preliminary evidence suggests that the ability of illumination cues to block escape learning deficits may be related to their to reduce contextual fear (Experiment 3). The implications of these data for conceptions of instrumental control and the role of fear in the etiology of effects of inescapable shock exposure are discussed.

The nature of the initial coping response and the learned helplessness effect

The availability of an effective coping response has been shown to attenuate the deleterious behavioral and physiological consequences of inescapable electric shock. In the current study, two groups of rats could escape tailshock by turning a wheel. When short-latency responses that appeared to be elicited by shock onset were permitted to terminate shock, rats subsequently failed to learn to escape in a shuttlebox and did not differ from rats which received an equivalent amount of inescapable shock. However, when a relatively long-latency response was required and short-latency responses were not allowed to affect shock, rats subsequently readily learned to escape in the shuttlebox. The implications of these results for explanations of the manner in which prior exposure to shock influences subsequent escape learning were discussed.

Effects of discrimination training on stimulus generalization in pigeons: Role of resistance to extinction and response-produced stimuli

In Experiment 1, two groups (n = 10) of pigeons received 17 sessions of TD (true discrimination) or ND (nondifferential) training with line angles. Seventeen sessions of SS (single stimulus) training with a wavelength preceded this training and two followed it. Subsequent wavelength generalization testing in extinction revealed a sharper TD than ND gradient. This slope difference was evident from the very first test stimulus presentation and remained stable throughout testing. As a consequence of substantial overtraining, there was no reduction of response strength and no sharpening of generalization during testing for either group. In Experiment 2, two groups (n = 16) of pigeons received 10 sessions of TD or PD (pseudodiscrimination) training with line angles, followed by four sessions of SS training with a single wavelength. During this training and in subsequent wavelength generalization testing in extinction, brief blackouts separated stimulus presentations. Again, the TD group yielded the sharper gradient. Although responding weakened and the gradients sharpened during the test, these effects were comparable in the two groups. Furthermore, gradients based on the percentage of trials with at least one response showed the same TD-PD slope difference. This finding indicates that differential control over responding by response-produced feedback is inadequate to account for the TD-PD difference in generalization slope. Both experiments indicate that a purported difference in resistance to extinction is also an inadequate explanation.