Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Opioids act centrally to modulate stress-induced decrease in luteinizing hormone in the rat.

F Petraglia, W Vale, C Rivier

    Endocrinology
    |December 1, 1986
    PubMed
    Summary
    This summary is machine-generated.

    Related Concept Videos

    You might also read

    Related Articles

    Articles linked to this work by shared authors, journal, and citation graph.

    Sort by
    Same author

    Efficacy of administration sequence: Sacituzumab Govitecan and Trastuzumab Deruxtecan in HER2-low metastatic breast cancer.

    British journal of cancer·2024
    Same author

    Adolescent alcohol exposure alters the rat adult hypothalamic-pituitary-adrenal axis responsiveness in a sex-specific manner.

    Neuroscience·2013
    Same author

    Relative importance of nitric oxide and carbon monoxide in regulating the ACTH response to immune and non-immune signals.

    Stress (Amsterdam, Netherlands)·2012
    Same author

    Does IL-6 release ACTH by exerting a direct effect in the rat anterior pituitary.

    Stress (Amsterdam, Netherlands)·2012
    Same author

    Brain stem catecholamines circuitry: activation by alcohol and role in the hypothalamic-pituitary-adrenal response to this drug.

    Journal of neuroendocrinology·2011
    Same author

    Selective inhibitors of nitric oxide synthase (NOS) implicate a constitutive isoform of NOS in the regulation of interleukin-1-induced ACTH secretion in rats.

    Endocrine·2010
    Same journal

    Loss of the calorie restriction response protein DEPP1 worsens diet-induced obesity.

    Endocrinology·2026
    Same journal

    Long Non-Coding RNAs Mediate Endocrine Signaling and Resistance in Prostate Cancer.

    Endocrinology·2026
    Same journal

    Repeated Chemogenetic Activation of C1 Catecholamine Neurons Reduces Subsequent Glucoprivic Responses and Mimics HAAF.

    Endocrinology·2026
    Same journal

    Postnatal exposure to maternal hypothyroidism leads to developmental delay and metabolic dysregulations in male mice.

    Endocrinology·2026
    Same journal

    Discovery proteomics identification of factors contributing to gonadotropin β expression.

    Endocrinology·2026
    Same journal

    3D genome architecture and epigenetic regulation of lineage identity in advanced prostate cancer.

    Endocrinology·2026
    See all related articles

    Stress activates endogenous opioid peptides (EOP) and corticotropin-releasing factor (CRF), inhibiting luteinizing hormone (LH) secretion. This study identifies beta-endorphin and dynorphin-A as key mediators in stress-induced LH suppression.

    Area of Science:

    • Neuroendocrinology
    • Reproductive Physiology
    • Stress Response

    Background:

    • Stress activates endogenous opioid peptides (EOP) and corticotropin-releasing factor (CRF).
    • Both EOP and CRF centrally administered decrease luteinizing hormone (LH) levels.
    • The specific roles of EOP systems in stress-induced LH inhibition remain unclear.

    Purpose of the Study:

    • To elucidate the involvement of different EOP systems in stress-induced LH secretion inhibition.
    • To determine the opioid receptor subtypes mediating these effects.
    • To investigate the role of the CRF/EOP pathway in LH regulation during stress.

    Main Methods:

    • Used immunoneutralization and pharmacological receptor blockade in castrated male rats.
    • Administered anti-EOP sera, EOP antagonists (beta-human END-(6-31), beta-funaltrexamine, ICI 154,129), and receptor antagonists (Mr1452 MS, Mr2266 BS).

    Related Experiment Videos

  • Induced stress via inescapable intermittent footshock and administered ovine CRF intracerebroventricularly.

    • Main Results:

    • Anti-beta-endorphin (END) and anti-dynorphin-A (DYN-A) serum, along with kappa- and mu-opiate receptor antagonists, reversed stress-induced LH decrease.
    • Beta-endorphin antagonists partially blocked stress-induced LH inhibition, while delta-antagonists and anti-enkephalin serum had no effect.
    • CRF-induced LH decrease was reversed by anti-beta-END serum and beta-END antagonist, suggesting CRF acts via the beta-END system.

    Conclusions:

    • Stress-induced inhibition of LH secretion involves beta-END and DYN-A systems acting on mu/epsilon- or kappa-opiate receptors.
    • Centrally administered CRF inhibits LH levels primarily through the activation of the beta-END system.
    • The central CRF/beta-END pathway is likely crucial for stress-induced suppression of reproductive functions.