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Chronic stress differentially regulates glucocorticoid negative feedback response in rats
K Mizoguchi1, M Yuzurihara, A Ishige
1Pharmacology Department, Central Research Laboratories, Tsumura and Co., 3586 Yoshiwara, Ami-machi, Inashiki-gun, 300-1192, Ibaraki, Japan. mizoguchi_kazushige@mail.tsumura.co.jp
Psychoneuroendocrinology
|May 5, 2001
Summary
Chronic stress alters the body's response to stress hormones. While acute stress hormone release is suppressed after chronic stress, basal hormone secretion becomes less responsive, potentially impacting depression.
Area of Science:
- Neuroendocrinology
- Stress Physiology
Background:
- Chronic stress is linked to depression and altered glucocorticoid feedback.
- The precise mechanisms of chronic stress on glucocorticoid regulation remain unclear.
Purpose of the Study:
- To investigate the impact of chronic stress on glucocorticoid feedback mechanisms in rats.
- To elucidate the neurobiological changes associated with chronic stress and glucocorticoid regulation.
Main Methods:
- Rats were subjected to chronic water immersion and restraint stress for four weeks.
- Plasma corticosterone (CORT) levels were measured after acute and chronic stress.
- Dexamethasone (DEX) suppression tests were performed.
- Hippocampal [3H]DEX binding and activator protein-1 (AP-1) responses were analyzed.
Main Results:
- Chronically stressed rats showed rapid CORT decrease after acute stress compared to controls.
- DEX suppressed stress-induced CORT in chronically stressed rats but not acutely stressed rats.
- DEX suppression of basal CORT was reduced in chronically stressed rats.
- Hippocampal [3H]DEX binding decreased, and AP-1 response to acute stress was abolished in chronically stressed rats.
Conclusions:
- Chronic stress induces a hypersuppressive state for stress-induced CORT secretion and a hyposuppressive state for basal CORT secretion.
- Glucocorticoid receptor downregulation in the hippocampus may underlie these altered feedback mechanisms.
- These adaptations may contribute to stress-induced neural abnormalities relevant to depression.