| Abstract: | In both experiments, naltrexone attenuated the baseline tail-flick latencies. This opioid analgesia maybe due to either restraint stress or a conditioned association between the context and the shock. In the first case, the restraint stress itself leads to an unconditioned activation of the opioid system, which is blocked by naltrexone. In the second case, the subjects associate the experimental context (i.e., the Plexiglas tube, odor, etc.) with the shock, forming a CS-US association. If so, then the context may function as a long duration CS which elicits an opioid CR. From this perspective, it is possible that a 300 s duration CS was not long enough to activate the opioid system. Examining this issue may show that an extended CS+, such as context, is a critical determinant of the form of the CR. On the other hand, restraint may be the cause of the opioid analgesia observed during baseline measurements. Further research is needed to elucidate the cause of this effect. Understanding the variables which determine the form of conditioned hypoalgesia could have ramifications in the management of chronic pain. Knowledge in this may eventually result in the use of conditioning techniques to elicit intrinsic pain modulation that is not susceptible to tolerance. |
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