Diurnal alteration in opiate effects on the hypothalamo-pituitary-adrenal axis: changes in the mechanism of action

Opioid control of the hypothalamo-pituitary-adrenocortical axis has a characteristic circadian rhythm (Kiem, Kanyicska, Stark and Fekete, 1987). To elucidate the mechanisms leading to circadian alterations of opioid control of the hypothalamo-pituitary-adrenocortical axis, and to look for the recept...

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Bibliographic Details
Published in:European journal of pharmacology 1995-01, Vol.272 (2), p.145-150
Main Authors: Kiem, Do Thanh, Fekete, Márton I.K., Makara, Gábor B.
Format: Article
Language:English
Subjects:
ACTH (adrenocorticotrophin)
Adrenals. Interrenals
Adrenocortical hormones. Regulation
Animals
Biological and medical sciences
Circadian Rhythm
Corticosterone
Corticosterone - metabolism
Corticotropin-Releasing Hormone - metabolism
Diurnal alteration
Fundamental and applied biological sciences. Psychology
Hypothalamo-Hypophyseal System - drug effects
Male
Morphine - pharmacology
Naloxone - pharmacology
Opioid mechanism
Pituitary-Adrenal System - drug effects
Prolactin
Prolactin - metabolism
Rats
Rats, Sprague-Dawley
Vertebrates: endocrinology
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Summary:Opioid control of the hypothalamo-pituitary-adrenocortical axis has a characteristic circadian rhythm (Kiem, Kanyicska, Stark and Fekete, 1987). To elucidate the mechanisms leading to circadian alterations of opioid control of the hypothalamo-pituitary-adrenocortical axis, and to look for the receptor type at which the p.m. inhibitory action of opioids occurs, we examined the effect of morphine at different doses and the interaction between naloxone and morphine at different times of day in intact male Wistar rats. In the morning: morphine (10 and 30 mg/kg s.c.) significantly increased corticosterone secretion, while 3 mg/kg s.c. had no effect. Naloxone in a dose of 2.5 mg/kg i.p. significantly antagonized the corticosterone-releasing effect of morphine, suggesting that the secretion of corticosterone induced by morphine is mediated via μ-opioid receptors. In the afternoon: basal plasma corticosterone levels were higher than those in the morning, and morphine caused a significant corticosterone increase only at the dose of 30 mg/kg, and had no effect in the dose of 10 mg/kg. Morphine significantly decreased corticosterone levels in the dose of 3 mg/kg. This inhibitory action lasted approximately 3 h after morphine injection and was able to inhibit the circadian evening rise of corticosterone. The effect of morphine and the interaction between naloxone and morphine on prolactin secretion remained unchanged from a.m. to p.m.; naloxone (2.5 mg/kg i.p.) which inhibited the 30 mg/kg morphine-induced corticosterone rise in the morning failed to antagonize the 3 mg/kg morphine-induced decrease of corticosterone secretion in the afternoon. A high dose of naloxone (10 mg/kg i.p.) effectively prevented the 3 mg/kg morphine-induced p.m. inhibition of corticosterone secretion. The results of this study point to dual mechanism(s) of opioid action on the hypothalamopituitary-adrenal axis: the a.m. stimulatory mechanism is naloxone-sensitive, while the p.m. inhibitory mechanisms is naloxone-resistant.
ISSN:0014-2999
1879-0712
DOI:10.1016/0014-2999(94)00639-O