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Related Experiment Videos

Stress induced changes in testis function.

A López-Calderón1, C Ariznavarreta, M I González-Quijano

  • 1Departamento de Fisiología, Facultad de Medicina, Universidad Complutense, Madrid, Spain.

The Journal of Steroid Biochemistry and Molecular Biology
|January 1, 1991
PubMed
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Chronic stress disrupts the hypothalamic-pituitary-testicular axis, lowering testosterone by altering luteinizing hormone-releasing hormone (LHRH) secretion, not pituitary response. Opioid blockers did not reverse this stress effect.

Area of Science:

  • Neuroendocrinology
  • Stress Physiology
  • Reproductive Biology

Background:

  • Chronic stress negatively impacts the hypothalamic-pituitary-testicular axis.
  • Stress-induced reductions in testosterone secretion are linked to decreased gonadotropin levels.

Purpose of the Study:

  • To investigate the mechanism by which chronic stress inhibits the hypothalamic-pituitary-testicular axis.
  • To determine the role of luteinizing hormone-releasing hormone (LHRH) secretion and pituitary responsiveness in stress-induced reproductive axis inhibition.
  • To explore the involvement of beta-endorphins and other opioids in this process.

Main Methods:

  • Chronic restraint stress was applied to rats.
  • Plasma testosterone and gonadotropin (LH, FSH) levels were measured.

Related Experiment Videos

  • Hypothalamic LHRH content and pituitary responsiveness to LHRH were assessed.
  • Beta-endorphin levels in the hypothalamus and pituitary were analyzed.
  • The effect of naltrexone (an opioid receptor antagonist) on gonadotropin levels was studied.

    • Main Results:

    • Chronic stress decreased plasma testosterone and gonadotropin levels.
    • Hypothalamic LHRH content was reduced, while pituitary response to LHRH was enhanced.
    • Pituitary beta-endorphin secretion increased, but hypothalamic levels remained unchanged.
    • Naltrexone administration did not alter the stress-induced decrease in LH and FSH.

    Conclusions:

    • Chronic stress inhibits the testicular axis primarily by altering hypothalamic LHRH secretion, not by reducing pituitary responsiveness.
    • The observed effects appear to be mediated by a non-opioid mechanism at the hypothalamic level.