Reversal of the action of morphine on the secretory activity of the adrenal cortex

Sablé-Amplis, R.; Agid, R; Abadie, Delphine

doi:10.1016/0006-2952(74)90576-0

Cited by 9 publications

(4 citation statements)

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“…During the winter, a significant 30% reduction in plasma CS was observed in rabbits 1 h after the injection of morphine, 10 mg/kg i.m. [33]. Significant de creases in plasma CS have also been reported after the acute intravenous administration of an enkephalin analog or methadone in nonaddicted humans [5,9,35].…”

Section: Discussionmentioning

confidence: 99%

“…p-EP is more potent than MS in causing the release of pituitary ACTH and P-EP. These findings are consistent with a role for brain endorphins in the regulation of CRF release.Since the initial discovery of Se/ye [34], numerous studies have confirmed that morphine activates the hypothalamicpituitary-adrenal (HPA) system in laboratory animals [4,7,19,21,26,27,33, 44]. It has also been shown that p-endorphin (P-EP) administration increases the secretion of ACTH in rats [38].…”

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confidence: 99%

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Effect of Intraventricular β-Endorphin and Morphine on Hypothalamic-Pituitary-Adrenal Activity and the Release of Pituitary β-Endorphin

Haracz¹,

Bloom²,

Wang³

et al. 1981

Neuroendocrinology

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The effects of intraventricular (i.v.t.) morphine sulfate (MS) and β-endorphin (β-EP) on pituitary-adrenal activity and the release of pituitary β-EP were studied in rats. Pituitary-adrenal activity was monitored by measuring plasma corticosterone (CS) levels. 45 min after i.v.t. injection, both MS and β-EP caused dose-related increases in plasma CS, with β-EP being approximately ten times more potent on a molar basis. MS injected i.v.t. at 0.3, 1.0, 3.0 and 10.0 μg did not cause a significant reduction in pituitary immunoreactive (i.r.) β-EP, but did cause an increase in plasma i.r. β-EP at 3 μg of MS. β-EP injected i.v.t. at 1.5 μg caused a reduction of pituitary i.r. β-EP. Since i.v.t.-injected β-EP may have contributed to the measured plasma i.r. β-EP, a nonimmunoreactive analog (Des-Asn²⁰-β_c-EP) was used to assess the change in plasma i.r. β-EP. 5 μg of Des-Asn²⁰-β_c-EP injected i.v.t. caused increases in plasma i.r. β-EP and CS, as well as a 40% reduction in pituitary i.r. β-EP. The concomitant intraperitoneal (i.p.) injection of naloxone HC1 (10 mg/kg) significantly blocked the increase in plasma CS induced by 5 μg of β-EP. When naloxone HC1, 10 mg/kg was injected alone, a significant increase in plasma CS was found. The results indicate that i.v.t. β-EP is more potent than MS in causing the release of pituitary ACTH and β-EP. These findings are consistent with a role for brain endorphins in the regulation of CRF release.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Effect of Intraventricular β-Endorphin and Morphine on Hypothalamic-Pituitary-Adrenal Activity and the Release of Pituitary β-Endorphin

Haracz¹,

Bloom²,

Wang³

et al. 1981

Neuroendocrinology

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“…Here we have demonstrated that a previous uncontrollable stressor enhances the CORT response to morphine as well, and that this response is necessary for the potentiation of morphine's rewarding effects as measured by CPP. It was already known that acute morphine elevates CORT levels in rodents (Sable-Amplis et al 1974), and given the low dose of morphine used here, it is not surprising that CORT was only slightly elevated following drug administration. However, the results from the first experiment demonstrate that an acute uncontrollable stressor, such as IS, potentiates the CORT response to the same dose of morphine.…”

Section: Discussionmentioning

confidence: 85%

“…Although the precise mechanism by which stress, and CORT more specifically, alters the rewarding effects of drugs is unknown, there is abundant evidence implicating CORT as a possible mediator of the interaction between stress and drugs of abuse. For example acute administration of psychostimulants (Knych and Eisenberg 1979), opiates (Sable-Amplis et al 1974), nicotine (Balfour et al 1975), or ethanol (Ellis 1966), have been shown to increase plasma CORT levels in rodents. Although acute morphine treatment decreases plasma CORT levels in humans (Allolio et al 1987), and chronic opiate and alcohol administration leads to the development of tolerance of the CORT response to these drugs in both rodents and humans (Spencer and McEwen 1990;Pechnick 1993;Kreek 1996).…”

Section: Introductionmentioning

confidence: 99%