The central representation of an aversive event maintains the opioid and nonopioid forms of analgesia.
Exposure to an aversive event, such as shock, can elicit either an opioid or nonopioid analgesia in rats. We suggest that the central representation of an aversive event in working memory activates both forms of analgesia. We formalize this basic hypothesis by coupling it with a current model of animal learning and memory, SOP (Wagner, 1981). SOP is designed to capture the standard operating procedures that govern memory systems. Our application of SOP suggests that manipulations which disrupt the maintenance of information in working memory should alter the magnitude and time course of analgesia. Three experiments are reported that support our proposal. Experiment 1 showed that analgesia decays more rapidly if the representation of the aversive event is displaced from working memory by presenting a postshock distractor. Experiment 2 demonstrated that the postshock distractor alters the magnitude and time course of both the opioid and nonopioid forms of analgesia. Experiment 3 demonstrated that pharmacologically disrupting working memory, by administering a high dose of pentobarbital, prevents mild shock from inducing a strong change in pain reactivity. Implications of the results are discussed.
D000818:Animals; D001143:Arousal / Q000502:physiology; D001288:Attention / Q000502:physiology; D001362:Avoidance Learning / Q000502:physiology*; D001921:Brain / Q000502:physiology; D008297:Male; D011939:Mental Recall / Q000502:physiology; D009271:Naltrexone / Q000494:pharmacology; D009433:Neural Inhibition / Q000187:drug effects; D009619:Nociceptors / Q000502:physiology*; D010424:Pentobarbital / Q000494:pharmacology; D051381:Rats; D011957:Receptors, Opioid / Q000502:physiology*; D013116:Spinal Cord / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects
D011957:Receptors, Opioid; D009271:Naltrexone; D010424:Pentobarbital