Long-Term Stress-Induced Analgesia and Activation of the Opiate System

Grau, James W.; Hyson, Richard L.; Maier, Steven F.; Madden, John J.; Barchas, Jack D.

doi:10.1126/science.7268445

Cited by 283 publications

(161 citation statements)

References 15 publications

(2 reference statements)

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“…This response may follow a period of active but unsuccessful engagement with a source of stress, and is characterized by quiescence, hypotension, decreased responsiveness to the environment, and prolonged opioid-mediated analgesia (Grau et al, 1981;Keay and Bandler, 2001;Ribeiro et al, 2005). In the present study high levels of discouragement apparently evoked opioid release which, in turn, 'capped' painful sensations during the final cold pressor test.…”

Section: Discussionmentioning

confidence: 55%

Negative affect, pain and sex: The role of endogenous opioids

Frew

Drummond

2007

Pain

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Opioid neurotransmission modulates pain and negative affect during psychological stress.To determine whether these effects differ between men and women, the opioid receptor antagonist naltrexone or placebo was administered double-blind to 21 men and 22 women before they completed 30 minutes of difficult mental arithmetic. To heighten negative affect, participants received seven moderately noxious electric shocks during the math task, which were believed to be contingent upon performance. Before and after the math task, participants rated pain intensity and unpleasantness while their left hand was immersed in 2 o C water for up to 4 minutes. Anxiety, discouragement and anger were also rated before, during and after the math task. Tolerance of cold-induced pain was greater in men, whereas discouragement during the math task was greater in women. Opioid blockade did not influence ratings of negative affect, which increased in line with the intensity and unpleasantness of shock-induced pain. The intensity and unpleasantness of cold-induced pain increased after the math task only in women administered naltrexone.Within the naltrexone condition, pain ratings increased most in the most discouraged subjects. However, this relationship was absent in placebo recipients, implying that the hyperalgesic effect of psychological distress was tempered by opioid release. Greater stress-evoked discouragement in women than men may explain why cold-induced pain increased after the math task only in women administered naltrexone.

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Section: Discussionmentioning

confidence: 55%

Negative affect, pain and sex: The role of endogenous opioids

Frew

Drummond

2007

Pain

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“…The effect of ADX is a long-lasting phenomenon persisting for a period as long as 7 or even 14 days. A similar long-term effect was obser ved also for stress-induced analgesia (15,20,21]. MacLennan et al [21] suggested that corticosterone is of critical im portance in the development of the long-term opioid form of stress-induced analgesia.…”

Section: Discussionmentioning

confidence: 64%

Long-Lasting Glucocorticoid Suppression of Opioid-Induced Antinociception

Ratka

Sutanto

Kloet³

1988

Neuroendocrinology

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The antinociceptive effect of morphine (5 mg/kg body weight i.p.) in rats subjected to various experimental manipulations of the pituitary-adrenocortical system was studied. The absence of adrenal steroids increased the sensitivity to morphine. The following findings suggest that glucocorticosteroids have a long-lasting influence on opioid-induced antinociception, even when the steroids have been removed by adrenalectomy. First, when rats were adrenalectomized in the morning under basal conditions of pituitary-adrenocortical activity (plasma corticosterone level < 1 µg%), the subsequent hypersensitivity to morphine was more pronounced than when rats were adrenalectomized in the evening (plasma corticosterone level 18.4 µg%). This difference in hypersensitivity to morphine-induced antinociception following adrenalectomy either in the morning or in the evening persisted for at least 2 weeks. Second, exposure to a novel environment (stress of a new cage) or administration of corticosterone (10 mg/kg body weight s.c.) prior to morning adrenalectomy decreased the sensitivity to morphine measured 1 week later. Third, RU 38486, a glucocorticoid antagonist, injected in the lateral cerebral ventricle prior to the evening adrenalectomy increased subsequent morphine antinociception. In attempts to understand the long-term effect on morphine antinociception, the opioid receptor sites were quantified by an in vivo procedure. Quantitative autoradiography of binding sites labeled after intravenous administration of a tracer dose of [³H]-diprenorphine showed a decrease in retention of the labeled opioid in cortical and midbrain regions of rats adrenalectomized in the evening when compared with rats operated in the morning. In conclusion, the data suggest that a neuroen-docrine state invoked by the actual plasma corticosterone level at the time of adrenalectomy has a long-lasting influence on the degree of post-adrenalectomy opioid-induced antinociception. These long-term alterations of opioid responsiveness are reflected in altered binding to the opioid receptor system in the brain.

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“…Furthermore, some kinds of stimulus-pro duced analgesia depend on the integrity of the adreno-hypophyseal axis [Watkins and Mayer, 1982] and stressful stimuli have been found to elicit long-lasting analgesic effects [Grau et al, 1981], Since amphetamine in duces release of both pro-opiomelanocortine derivatives from adenohypophysis and of glucocorticoids from adrenal cortex, [Brown et al, 1978;Knych andEisenberg, 1980;Co hen et al. 1981], we also tested the possibility that cathinone is a pharmacological equiva lent of stress in eliciting analgesia.…”

Section: Introductionmentioning

confidence: 99%

Prolonged Analgesia Induced by Cathinone

Nencini¹,

Ahmed²,

Anania³

et al. 1984

Pharmacology

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Cathinone, the active principle of Catha edulis (khat), shows long-lasting analgesic effects when the tail-flick test is used in rats. The involvement of monoamines, endogenous opioids and stress in this analgesic effect was tested. Both early (30 min) and late (24 h) analgesic effects of cathinone were prevented by reserpine or p-chlorophenylalanine, which deplete catecholamines or serotonin, respectively, and by nomifensine, which prevents neuronal uptake of biogenic amines and amphetamines. The same inhibitory effect was obtained with a high dose (4 mg/kg) of naloxone. However, rats made tolerant to morphine retained both early and late analgesic response to cathinone. The increase in plasma ACTH induced by the tail-flick test at 30 min and 24 h was significantly enhanced by cathinone, in a naloxone-reversible way. However, the analgesic responses shown at these times were not prevented by either dexamethasone or adrenalectomy. We conclude that the prolonged analgesia induced by cathinone is primarily due to an amphetamine-like activation of monoaminergic pathways, but requires the integrity of non-μ-opioid mechanisms. The involvement of the adrenohypophyseal axis in this cathinone effect is less probable.

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Long-Term Stress-Induced Analgesia and Activation of the Opiate System

Cited by 283 publications

References 15 publications

Negative affect, pain and sex: The role of endogenous opioids

Negative affect, pain and sex: The role of endogenous opioids

Long-Lasting Glucocorticoid Suppression of Opioid-Induced Antinociception

Prolonged Analgesia Induced by Cathinone

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