Fos-like immunoreactivity in the rat hypothalamic-pituitary axis after immobilization stress

J Kononen1, J Honkaniemi, H Alho

  • 1Department of Biomedical Sciences, University of Tampere, Finland.

Endocrinology
|May 1, 1992
PubMed

Insights

Immobilization stress increases c-fos expression in the rat brain and pituitary. Glucocorticoids reduce this stress response in the pituitary but not the hypothalamus, indicating a complex regulatory role.

Area of Science:

  • Neuroscience
  • Endocrinology
  • Molecular Biology

Background:

  • The protooncogene c-fos is rapidly expressed in response to various stimuli.
  • Stress response involves complex neuroendocrine pathways.
  • The pituitary and hypothalamus are key regulators of the stress response.

Purpose of the Study:

  • To investigate the effect of immobilization stress on c-fos expression in the rat pituitary and hypothalamus.
  • To determine the role of glucocorticoids in modulating stress-induced c-fos expression.

Main Methods:

  • Immunohistochemistry was used to detect Fos-like immunoreactivity (Fos-LI).
  • Antibodies against c-fos protein (Fos) were utilized.
  • Double-staining identified Fos-immunoreactive cells containing corticotropin.
  • Dexamethasone was administered to assess glucocorticoid effects.

Main Results:

  • Immobilization stress significantly increased Fos-LI in the hypothalamus (paraventricular nucleus) and pituitary (anterior and intermediate lobes).
  • The majority of Fos-immunoreactive pituitary cells contained corticotropin.
  • Dexamethasone pretreatment reduced stress-induced Fos-LI in the pituitary but not the hypothalamus.
  • Glucocorticoids did not directly repress c-fos expression in the paraventricular nucleus.

Conclusions:

  • Immobilization stress induces c-fos expression in both the hypothalamus and pituitary.
  • Fos may regulate mediators of the stress response, including CRF and POMC-derived peptides.
  • Glucocorticoids appear to indirectly modulate pituitary c-fos expression, possibly via reduced CRF release.

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