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

Haracz, John L.; Bloom, Alan S.; Wang, R.I.H.; Tseng, Leon F.

doi:10.1159/000123224

Cited by 57 publications

(12 citation statements)

References 27 publications

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“…Opiates are believed to play an important role in the control of the HPA. In rats, acute administration of both morphine and its antagonist, naloxone results in HPA axis activation [18, 19], while repeated morphine treatment can cause chronic stress symptoms [20,21,22]. …”

Section: Introductionmentioning

confidence: 99%

Stress Symptoms Induced by Repeated Morphine Withdrawal in Comparison to Other Chronic Stress Models in Mice

et al. 2005

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The present study was aimed at evaluating chronic stress models in mice with special attention to morphine treatment. We hypothesized that repeated periods of drug withdrawal induce chronic stress. To verify this hypothesis, mice were made dependent on morphine and then subjected to several types of repeated withdrawal. Body weight reduction, thymus involution, adrenal gland enlargement and activation of the hypothalamo-pituitary-adrenal axis were used as signs of chronic stress. The changes were compared to those induced by ‘laboratory’ models of chronic stress (2 weeks of repeated restraint or rat exposure) and to a disease model of streptozotocin-induced diabetes mellitus (STZ-DM). Mice were made dependent using increasing doses of morphine three times a day for 3 days (10–20–40 mg/kg s.c.). Thereafter, withdrawal was induced either spontaneously (morphine 40 mg/kg injected at 24- or 72-hour time intervals for 2 weeks) or repeatedly precipitated by naloxone (10 mg/kg s.c.) injected daily 3 h after morphine. The results show that repeated periods of spontaneous drug withdrawal (24 or 72 h) in morphine-dependent mice represent a mild stress load. Repeated withdrawal precipitated by naloxone induced clear chronic stress-like changes. Changes observed in the naloxone-precipitated withdrawal model were even more pronounced than those found in laboratory models, namely repeated restraint or exposure to the rat. The most severe chronic stress state developed in mice during untreated STZ-DM. Thus, naloxone-precipitated withdrawal in mice seems to be an appropriate model of chronic stress.

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Section: Introductionmentioning

confidence: 99%

Stress Symptoms Induced by Repeated Morphine Withdrawal in Comparison to Other Chronic Stress Models in Mice

et al. 2005

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“…Several effects of opioid peptides and opioid drugs on the neuro-endocrine system have been rather well established [for reviews, see 18, 30], Thus, in addition to the regulatory effects of DA and NA mentioned above, also opioids have been reported to affect the secretion of LH [31,38,53,58] and prolactin [25,58]. Moreover, the hypo thalamus-pituitary-adrenocortical axis, involved in stress re sponses, appears to be stimulated by morphine [2,3,13] as well as other opioid agonists [9,19]. However, little is known about the possible mechanisms (either direct or via modulation of monoamine release) by which opioids exert their effects on hor monal processes.…”

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confidence: 99%

Opioid-Receptor-Mediated Inhibition of [<sup>3</sup>H]Dopamine but Not [<sup>3</sup>H]Noradrenaline Release from Rat Mediobasal Hypothalamus Slices

Heijna

Padt²,

Hogenboom³

et al. 1991

Neuroendocrinology

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The modulation of the electrically evoked release of [³H]dopamine (DA) and [³H]noradrenaline (NA) by opioid receptor activation was examined in superfused slices of rat mediobasal hypothalamus (MBH). [³H]DA release was inhibited (maximally by 30–35%) by both the selective ĸ-agonist U 50,488 (1 nM to 1 µM) and the selective µ-agonist DAGO (0.01–1 µM) but not by the δ-selective agonist DPDPE (1 µM). Naloxone partly antagonized the inhibitory effect of U 50,488 and completely that of DAGO, whereas the selective K-antagonist norbinaltorphimine (nor-BNI) only antagonized the inhibition caused by U 50,488. The dopamine D₂ receptor agonist quinpirole as well as the α₂-adrenoceptor agonist oxymetazoline both decreased (by 25–30%) the evoked overflow of [³H]DA. The evoked release of [³H]NA was not modulated by any of the opioid agonists nor by quinpirole. However, the α₂-adrenoceptor agonist oxymetazoline inhibited the release of [³H]NA by 30–40%. Activation of α₂-adrenoceptors by oxymetazoline prevented the inhibitory effect of U 50,488, but not DAGO, on evoked [³H]DA release, whereas the selective K-antagonist nor-BNI antagonized the inhibition by oxymetazoline of [³H]DA, but not [³H]NA, release. In conclusion, activation of both ĸ- and µ-opioid receptors results in an inhibition of evoked DA release from MBH slices but does not modulate NA release. Therefore, several of the reported effects of opioids on hormone secretion may be an (indirect) consequence of a reduction of DA release. Moreover, the results suggest that activation of α₂-adrenoceptors inhibits DA release indirectly by stimulating release of endogenous opioids (probably dynorphins) which in turn inhibit evoked DA release by activation of K receptors.

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“…Some reports have demonstrated that morphine-induced increase in SCS levels is also mediated by the central nervous system. For example, increase in plasma corticosterone levels was produced by intraventricular (25) or intrahypothalamic injection (26) of morphine, and the effect of morphine on the hypothalamicpituitary-adrenal (HPA) axis was absent in hypothalamic lesioned (27) and hypophysectomized (28) rats. In vitro studies also demonstrated that morphine stimulated secretion of corticotropin-releasing factor (CRF) in the isolated hypothalamus but not of adrenocorticotropic hormone (ACTH) in the pituitary segments (29).…”

Section: Discussionmentioning

confidence: 99%

Involvement of Peripheral Mechanism in the Verapamil-Induced Potentiation of Morphine Analgesia in Mice

et al. 2004

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Abstract. Morphine's analgesic actions are thought to be mediated through both the central and peripheral nervous systems. L-type calcium channel blockers have been reported to potentiate the analgesic effects of morphine, but the locus of this interaction is not known. In this experiment, we examined the site of verapamil-induced potentiation of morphine analgesia in mice using the quaternary opioid receptor antagonist naloxone-methiodide (NLX-M). Subcutaneous injections of morphine increased locomotor activity and serum corticosterone level, which are mediated by the central nervous system. These central effects were not antagonized by 0.1 mg / kg of NLX-M, whereas this dose of NLX-M partially antagonized the analgesic effect of morphine. Treatment with verapamil potentiated morphine analgesia in a dosedependent manner. The verapamil-induced potentiation of morphine analgesia was abolished by pretreatment with NLX-M (0.1 and 1 mg/ kg). These findings suggest that peripheral mechanisms partially contribute to morphine analgesia and mediate the potentiation of morphine analgesia by verapamil.

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

Cited by 57 publications

References 27 publications

Stress Symptoms Induced by Repeated Morphine Withdrawal in Comparison to Other Chronic Stress Models in Mice

Stress Symptoms Induced by Repeated Morphine Withdrawal in Comparison to Other Chronic Stress Models in Mice

Opioid-Receptor-Mediated Inhibition of [<sup>3</sup>H]Dopamine but Not [<sup>3</sup>H]Noradrenaline Release from Rat Mediobasal Hypothalamus Slices

Involvement of Peripheral Mechanism in the Verapamil-Induced Potentiation of Morphine Analgesia in Mice

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