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Systemic ethanol administration elevates deoxycorticosterone levels and chronic ethanol exposure attenuates this
Rahul T Khisti1, Kevin N Boyd, Sandeep Kumar
1Department of Psychiatry and Pharmacology, Bowles Center for Alcohol Studies, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7178, USA.
Brain Research
|June 7, 2005
Summary
Acute ethanol intake boosts deoxycorticosterone (DOC) levels in rats. However, chronic ethanol consumption leads to tolerance, reducing this effect and impacting neurosteroid levels.
Area of Science:
- Neuroscience
- Endocrinology
- Pharmacology
Background:
- Systemic ethanol administration elevates GABAergic neuroactive steroid 3alpha,5alpha-THDOC levels.
- 3alpha,5alpha-THDOC is synthesized from deoxycorticosterone (DOC) via adrenal and brain metabolism.
Purpose of the Study:
- Investigate deoxycorticosterone (DOC) levels in plasma and brain following ethanol administration in rats.
- Compare DOC levels in ethanol-naïve versus chronically ethanol-exposed rats.
Main Methods:
- Rats were administered ethanol (2 g/kg, i.p.) or saline.
- DOC levels were quantified in plasma and various brain regions using radioimmunoassay.
- Chronic ethanol exposure involved a 15-day ethanol liquid diet followed by an ethanol challenge.
Main Results:
- Ethanol administration significantly increased DOC levels in plasma and brain regions (cerebral cortex, hippocampus, hypothalamus, cerebellum, olfactory tubercle) of naïve rats.
- A 2-week chronic ethanol consumption followed by an ethanol challenge resulted in an attenuated elevation of DOC in plasma and brain.
- These results indicate acute ethanol increases DOC, while chronic consumption induces tolerance to this effect.
Conclusions:
- Acute ethanol exposure increases deoxycorticosterone (DOC) levels in ethanol-naïve rats.
- Chronic ethanol consumption leads to tolerance in the ethanol-induced elevation of DOC levels.
- Findings suggest adaptive changes in DOC regulation with sustained ethanol intake.