title: The analgesic response to stress: genetic and gender considerations.
abstract: The brain contains neuronal circuits, activation of which by electrical stimulation or environmental stress causes analgesia. Both opioid and non-opioid forms of stimulus-induced analgesia exist, and are anatomically differentiated. Several transmitters have been postulated for non-opioid stimulus-induced analgesia, N-methyl-D-aspartic acid being a particularly likely candidate. In mice there are marked gender differences in the underlying neurochemical medication of stress-induced analgesia, the development of which is sensitive to the hormonal environment during early post-natal development and which changes with age in both sexes. Mice can be bred for a high or low analgesic response to stress and there is evidence that this is determined by a single gene. Operative pain, as a stressor, inhibits natural killer (NK) cell activity and influences the propensity to develop metastases when mice are inoculated with an experimental tumour after abdominal surgery. This can be influenced by peri-operative morphine in analgesic doses.
authors.affiliation: Department of Psychology, University of California, Los Angeles 90005-1563, USA.
authors.forename: W F
authors.initials: WF
authors.lastname: Sternberg
authors.forename: J C
authors.initials: JC
authors.lastname: Liebeskind
mesh_terms: D000375:Aging / Q000502:physiology; D000698:Analgesia; D000818:Animals; D005260:Female; D008297:Male; D051379:Mice; D018377:Neurotransmitter Agents / Q000502:physiology; D010146:Pain / Q000235:genetics* / Q000503:physiopathology*; D012727:Sex Characteristics; D013312:Stress, Physiological / Q000503:physiopathology*
chemical_list: D018377:Neurotransmitter Agents