Although exposure to inescapable shocks induced analgesia in rats, the analgesia was not manifest 24 hours later. A brief reexposure to shock, however, restored the analgesia. This reexposure to shock had an analgesic effect only if the rats had been shocked 24 hours previously. Further, long-term analgesic effects depended on the controllability of the original shocks and not on shock exposure per se. Implications of these results for learned helplessness and stress-induced analgesia are discussed.

These experiments explored whether exposure to inescapable shock produces a subsequent deficit in the organism's 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.

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Five experiments examined the influence ot opiate antagonists on both the short-term analgesic reaction resulting 30 min after exposure to inescapable shock and the long-term analgesic reaction resulting after reexposure to shock 24 hr after inescapable shock exposure. Experiment 1 showed that the longterm analgesic reaction could be reduced by administration of naltrexone prior to exposure to inescapable tail shock. Experiment 2 showed that the reduction in the long-term analgesic reaction produced by naltrexone was dosedependent. Experiment 3 showed that the long-term analgesic reaction could also be reduced by administration of naltrexone prior to reexposure to shock. Experiment 4 showed that the long-term analgesic reaction could be reduced by administration of a large dose of naloxone prior to reexposure to shock. Experiment 5 showed that the short-term analgesic reaction was reduced by naltrexone administered prior to inescapable shock. Some implications of these results for the biochemical substrates of both learned helplessness and stress-induced analgesia are discussed.Exposure to inescapable and unavoidable aversive events has widespread behavioral and physiological consequences (see Maier & Seligman, 1976, for a review). Under some conditions, organisms exposed to inescapable and unavoidable electric shocks later show poor learning to escape shock in a different situation in which escape is possible (the so-called "learned helplessness effect"; cf. Overmier & Seligman, 1967), reduced activity in the presence of shock