Stress-induced analgesia: A performance deficit or a change in pain responsiveness?1
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Cited by (13)
Pain control in tonic immobility (TI) and other immobility models
2022, Progress in Brain ResearchCitation Excerpt :After a single episode of restraint, locomotor activity displays species-specific modifications (no change, increase and decrease) (Porro and Carli, 1988). In rats for instance, 30 min of restraint in a snug-fitting Plexigas apparatus increases escape latency without affecting the motor activity in the open field test: restraint affects nociceptive responsiveness but not motor performance (Blair et al., 1982). There is evidence that restraint-induced analgesia in rats is dependent on the endogenous opiates of peripheral origin, i.e., pituitary and adrenals.
The Neuronal Circuit Between Nociceptin/Orphanin FQ and Hypocretins/Orexins Coordinately Modulates Stress-Induced Analgesia and Anxiety-Related Behavior
2015, Vitamins and HormonesCitation Excerpt :SIA plays a role in adaptation to threats and is a component of the defensive behavioral response to prepare for “fight or flight.” However, exaggerated or prolonged SIA phenomenon has been regarded as a performance deficit (Blair, Galina, Holmes, & Amit, 1982). Recently it has been suggested SIA may serve as a measure of stress severity and as a model of “depersonalization disorder” in humans.
Direct inhibition of hypocretin/orexin neurons in the lateral hypothalamus by nociceptin/orphanin FQ blocks stress-induced analgesia in rats
2011, NeuropharmacologyCitation Excerpt :Unlike the wildtype mice, the orexin/ataxin-3 mice did not exhibit the thermal pain threshold increase caused by restraint stress, while acute analgesia was induced by i.c.v. administration of Hcrt-1 (Xie et al., 2008). Although SIA is a natural stress-induced neuroadaptation, exaggerated or prolonged SIA phenomenon has been regarded as a performance deficit (Blair et al., 1982; Amit & Galina, 1986). It has been suggested that SIA might serve as a measure of stress severity and a model of ‘depersonalization disorder’ in humans (Kenunen & Prakh’e IV, 2005; Kenunen et al., 2006).
Delayed nociceptive response following cold-water swim in the formalin test: Possible mechanisms of action
1996, Experimental Neurology
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We would like to thank Mr. Ralph Berman and Brett—Pat Canada Ltd. for their financial support of this research. These experiments were also supported in part from an NSERC grant to Zalman Amit.