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Decreased sensitivity to glucocorticoid fast feedback in chronically stressed rats
E A Young1, S Akana, M F Dallman
1Mental Health Research Institute, University of Michigan, Ann Arbor.
Neuroendocrinology
|May 1, 1990
Summary
Chronic stress and corticosterone treatment block fast and delayed feedback mechanisms in rats, potentially due to reduced hippocampal glucocorticoid receptors. This impacts stress hormone regulation.
Area of Science:
- Neuroendocrinology
- Stress Physiology
Background:
- Chronic stress induces changes in anterior pituitary corticotrophs, including increased ACTH and beta-endorphin.
- Glucocorticoid negative feedback on stress hormone secretion is impaired following chronic stress.
Purpose of the Study:
- To investigate if in vitro observed changes in glucocorticoid feedback after chronic stress are also present in vivo.
- To examine the effects of chronic footshock and corticosterone treatment on fast feedback mechanisms.
Main Methods:
- Development of a fast feedback paradigm using swim stress and corticosterone injection.
- Assessment of ACTH and beta-endorphin responses to stress and feedback inhibition in rats subjected to chronic footshock or corticosterone treatment.
Main Results:
- Corticosterone effectively inhibited stress-induced ACTH and beta-endorphin responses in control rats.
- This fast feedback inhibition was abolished in rats exposed to chronic footshock or daily corticosterone treatment for 14 days.
- Fast feedback was intact in rats exposed to a less intense swim stress paradigm.
Conclusions:
- Both fast and delayed feedback mechanisms of corticosterone are impaired by high levels of chronic stress.
- Chronic corticosterone treatment may also block these feedback systems, possibly by reducing hippocampal glucocorticoid receptor number.