Range of environmental stimuli producing nociceptive suppression: implications for neural mechanisms.
Initial studies of environmentally induced analgesia in the rat established several important characteristics of this phenomenon. We demonstrated that stressful environmental stimuli were not sufficient to produce nociceptive suppression. However, emphasis by many researchers on stress-related analgesia has limited studies of the range of environmental contexts producing nociceptive suppression and handicapped efforts to describe neural mechanisms mediating EIA. Another feature of EIA was the observation that the nervous system might contain multiple opiate and non-opiate systems capable of modulating nociceptive responses. Although previous research had recognized the possibility of endogenous opiate analgesic systems, little attention had been given to non-opiate analgesic mechanisms. Since it seems unlikely that multiple systems would serve purely redundant roles, it seemed reasonable to speculate that at least some of these systems may mediate other modulatory functions in addition to regulating sensory information on noxious stimuli. The observation that some environmental conditions could increase nociceptive responses certainly indicated that environmentally induced nociceptive modulation was not restricted to analgesia. These and other observations lead us to suspect that neural mechanisms mediating at least some forms of EIA could be related to mechanisms mediating more general modulating processes associated with selective attention, orienting, or arousal. Subsequent studies in the primate established that changes in vigilance demands, stimulus relevance, and stimulus predictability could modulate responses of medullary dorsal horn nociceptors coding sensory-discriminative information on noxious thermal stimuli. However, these studies provided no information on the neural mechanisms mediating this modulation. Later studies in cats described an endogenous, non-narcotic analgesic system representing a subcomponent of a larger cholinergic system principally involved in regulating animals' responsiveness to external stimuli. Research also indicated that this cholinergic analgesic system could function physiologically to modulate nociceptive responsiveness in the presence of certain environmental stimuli but not others. Considered together, data from these studies indicate that, while stress is not sufficient to produce analgesia, a variety of environmental conditions can modulate nociceptive input. A number of different neural systems could contribute EIA associated with various stimuli. It is possible that the regulation of nociceptive input is not the exclusive, or even principal, consequence of normal activity within certain of these systems.
D000698:Analgesia; D000818:Animals; D001143:Arousal; D001285:Atropine / Q000494:pharmacology; D001522:Behavior, Animal; D001921:Brain / Q000502:physiology; D002415:Cats; D008845:Microinjections; D009474:Neurons / Q000502:physiology; D009619:Nociceptors / Q000502:physiology*; D010812:Physical Stimulation; D051381:Rats; D013116:Spinal Cord / Q000502:physiology; D013312:Stress, Physiological / Q000503:physiopathology
D001285:Atropine