Central mechanisms of pain modulation.
Bulbospinal serotonergic neurons and two physiological classes of bulbospinal nonserotonergic cells interact to modulate pain transmission. Recent studies have begun to elaborate targets of descending pain modulation other than the well-studied flexion withdrawal pathways. Site-specific, naloxone-sensitive placebo analgesia, which is hard to reconcile with current models of descending pain modulation, presents an exciting challenge to the field.
Mason
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Department of Neurobiology, Pharmacology and Physiology, Committee on Neurobiology, The University of Chicago, 947 East 58th Street, Chicago, Illinois 60637, USA. pmason@midway.uchicago.edu
D000700:Analgesics / Q000494:pharmacology*; D000818:Animals; D005727:Ganglia, Spinal / Q000187:drug effects / Q000502:physiology; D009020:Morphine / Q000494:pharmacology; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology*; D009619:Nociceptors / Q000187:drug effects / Q000502:physiology*; D010147:Pain Measurement / Q000187:drug effects*; D011903:Raphe Nuclei / Q000187:drug effects / Q000502:physiology*; D012701:Serotonin / Q000502:physiology; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*; D013116:Spinal Cord / Q000187:drug effects / Q000502:physiology
D000700:Analgesics; D009292:Narcotic Antagonists; D012701:Serotonin; D009270:Naloxone; D009020:Morphine