Development of Shock-Induced Analgesia: A Search for Hyperalgesia

With the use of parameters intended to maximize the potential to observe hyperalgesia, the possibility was examined that hyperalgesia might be the immediate response to aversive stimulation, whereas analgesia is delayed (Matzel & Miller, 1987). Consistent with the later prediction, analgesia in rats, as assessed by latency to paw lick in response to thermal stimulation, increased as a function of the delay between a tailshock (Experiment 1) or footshock (Experiment 3) and the test of pain sensitivity. However, in neither case was a hyperalgesic response observed at shock offset. In Experiment 2, the strength of the analgesic response was found to increase as a direct function of both the time since the tailshock and tailshock intensity over the limited ranges examined, but no hyperalgesia was observed immediately after either low- or highintensity shock. In Experiment 4, the opiate antagonist naloxone was found to attenuate both a weak immediate and stronger delayed analgesia, results suggesting a common underlying mechanism. This mitigates the likelihood that differential behavioral responses at short and long delays following shock were obscuring hyperalgesia at the time of shock offset or were summating with an analgesic response at the long delay to create the impression of enhanced analgesia. In total, these experiments provide evidence that opioid analgesia mediates a compensatory process that increases over time, but they provide no evidence that pain sensitivity increases above baseline levels immediately following an aversive event. These data are discussed in relation to preparatory models of endogenous analgesic functioning and the role of endogenous opioids in learning.