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Related Experiment Videos

Decrease of morphine-induced prolactin release by a procedure causing prolonged stress.

M I Fekete, B Kanyicska, T Szentendrei

    The Journal of Endocrinology
    |May 1, 1984
    PubMed
    Summary
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    Stress and cortisol prolongedly inhibit opioid drug effects on prolactin. This suggests stress alters opioid neuromodulation through glucocorticoid release, impacting hormone secretion.

    Area of Science:

    • Neuroendocrinology
    • Pharmacology
    • Stress Physiology

    Background:

    • Opioid drugs like morphine and fentanyl modulate prolactin secretion.
    • Stressful conditions can alter neuroendocrine responses to pharmacological agents.
    • Glucocorticoids are key stress hormones with known effects on the central nervous system.

    Purpose of the Study:

    • To investigate the impact of prolonged stress and exogenous cortisol on the prolactin-releasing effects of morphine and fentanyl in rats.
    • To determine if stress or cortisol alters the prolactin response to a non-opioid stimulus (haloperidol).

    Main Methods:

    • Rats were subjected to a 5-hour immobilization stress procedure.
    • Plasma prolactin levels were measured after administration of morphine, fentanyl, or haloperidol.

    Related Experiment Videos

  • The effects of a high dose of cortisol (25 mg/kg) on morphine-induced prolactin release were assessed.

    • Main Results:

    • Prolonged immobilization stress inhibited the prolactin increase induced by morphine and fentanyl.
    • Stress did not affect haloperidol-induced prolactin secretion.
    • Administration of a high cortisol dose also inhibited morphine-induced prolactin release, with maximal effect 24 hours post-injection.

    Conclusions:

    • Prolonged stress can lead to a sustained inhibition of opioid-mediated prolactin release in rats.
    • Glucocorticoid release, triggered by stress, appears to be a mechanism underlying this prolonged alteration in opioid neuromodulation.
    • These findings highlight the complex interplay between stress, glucocorticoids, and opioid systems in regulating endocrine function.