Rats were given series of escapable shocks, identical inescapable shocks, or no shock. The subjects were reexposed to a small amount of shock 24 hours later, after which an in vitro measure of the cellular immune response was examined. Lymphocyte proliferation in response to the mitogens phytohemagglutinin and concanavalin A was suppressed in the inescapable shock group but not in the escapable shock group. This suggests that the controllability of stressors is critical in modulating immune functioning.

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Exposure to painful or stressful stimuli produces an analgesic reaction which can persist for 1-2 h post-stress. In the typical stress-induced analgesia study the subject is not permitted to alter or exert control over the aversive event to which it is exposed. That is, its behavior affects neither the duration or intensity of the event. The experiments reported here attempted to determine whether this inability of the subject to control the aversive event is an important determinant of stress-induced analgesia, or whether simple exposure to painful events is a sufficient condition for its production. In the first experiment rats were given either escapable electric shocks (the subject's behavior could terminate the shock), equal amounts of inescapable shock, or no shock. Tail-flick to radiant heat was assessed 30 min later. The group given inescapable shock was strongly analgesic, while the group given an equal amount of escapable shock was only mildly analgesic. Thus the controllability of the shock or the availability of a coping response determined the antinociceptive reaction which followed. The second experiment revealed that this differential effect of controllability on tail-flick responding is masked, shortly after the end of the shock session, by a transient analgesic effect of shock which is not sensitive to the controllability dimension. The implications of these results for stress-induced analgesia and the activation of opioid systems are discussed.