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Published on: September 21, 2011
Testosterone is required for corticosteroid-binding globulin upregulation by morphine to be fully manifested
1Department of Psychiatry, Anatomy, and Neurobiology, Washington University School of Medicine, St. Louis, MO 63110, USA. bruce@dcm.wustl.edu
Pharmacology, Biochemistry, and Behavior
|December 13, 2000
Summary
Morphine increases corticosteroid-binding globulin (CBG) in male rats, an effect dependent on testosterone. Castration raises CBG levels, diminishing morphine
Area of Science:
- Endocrinology
- Neuropharmacology
- Molecular Biology
Background:
- Morphine elevates corticosteroid-binding globulin (CBG) in male rats, but not females, suggesting androgen dependence.
- Previous findings indicated a significant sexual dimorphism in morphine's effect on CBG concentrations.
Purpose of the Study:
- To investigate the role of androgens, specifically testosterone, in morphine-induced upregulation of corticosteroid-binding globulin (CBG).
- To determine if the opioid system mediates morphine's effect on CBG levels.
Main Methods:
- Surgical castration was performed on male rats at different life stages (pre-puberty, post-puberty, adulthood).
- Rats were treated with morphine or naltrexone, and testosterone replacement therapy was administered.
- Blood samples were analyzed to measure corticosteroid-binding globulin (CBG) concentrations.
Main Results:
- Castration significantly increased CBG concentrations in adult male rats, irrespective of the timing of the procedure.
- Morphine exposure increased CBG levels in intact male rats by approximately 100%.
- Testosterone replacement prevented the castration-induced rise in CBG and maintained the significant difference between placebo and morphine-treated groups.
Conclusions:
- Testosterone is essential for the full manifestation of morphine's effect on corticosteroid-binding globulin (CBG) levels in male rats.
- The observed increase in CBG following castration is not mediated by endogenous opioid release.
- Androgen status critically modulates the neuroendocrine response to morphine concerning CBG regulation.
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