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Published on: October 10, 2012
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.
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.
Abstract:
The effect of immobilization stress on the expression of the protooncogene c-fos in the rat pituitary and hypothalamus was investigated immunohistochemically using different polyclonal antibodies raised against the c-fos protein (Fos). After a 4 h immobilization, Fos-like immunoreactivity (Fos-LI) increased substantially in the parvocellular part of the paraventricular nucleus and in the intermediate and anterior lobe of the pituitary. The majority of the Fos-immunoreactive cells in the pituitary contained corticotropin, which was demonstrated by immunohistochemical double-staining. Since the paraventricular nucleus contains a large number of glucocorticoid receptor immunoreactive cells, the effect of a synthetic glucocorticoid, dexamethasone, on the induction of Fos-LI was studied. Dexamethasone treatment before immobilization considerably reduced the stress-induced expression of Fos-LI in the anterior and intermediate lobe of the pituitary but did not alter the induction of Fos-LI in the paraventricular nucleus. The present results demonstrate that immobilization stress induces Fos-LI both in the hypothalamus and in the pituitary, suggesting that Fos may be involved in regulating the synthesis of different mediators of stress response, such as CRF- and POMC-derived peptides. Apparently glucocorticoids do not directly repress c-fos expression, since dexamethasone did not affect the induction of Fos-LI in the paraventricular nucleus. The reduction of stress-induced Fos-LI in the pituitary by dexamethasone is possibly due to the diminished release of CRF factor from the paraventricular neurons.

