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Forebrain circumventricular organs mediate captopril-enhanced ethanol intake in rats
1Department of Psychology, University of Washington, Seattle 98195.
Pharmacology, Biochemistry, and Behavior
|August 1, 1993
Summary
Low-dose captopril increases ethanol intake in rats by acting on the brain. Lesions to the subfornical organ (SFO) abolished this effect, highlighting the SFO's critical role in captopril-enhanced drinking behaviors.
Area of Science:
- Neuroscience
- Pharmacology
- Physiology
Background:
- Angiotensin-converting enzyme (ACE) inhibitors, like captopril, are known to influence fluid intake.
- Chronic low-dose captopril administration enhances the intake of water, saline, and dilute ethanol solutions in rats.
Purpose of the Study:
- To investigate the role of the subfornical organ (SFO) and the organum vasculosum laminae terminalis (OVLT) in captopril-enhanced ethanol consumption.
- To elucidate the neural mechanisms underlying captopril's effects on ethanol intake.
Main Methods:
- Rats received subcutaneous infusions of captopril (5 mg/day for 14 days).
- Electrolytic lesions were made in either the SFO or the OVLT.
- Ethanol (6% v/v) intake was measured following captopril treatment and/or lesions.
Main Results:
- SFO lesions completely abolished the enhanced ethanol intake induced by captopril.
- OVLT lesions temporarily reduced captopril-enhanced ethanol intake.
- The SFO is demonstrated to be essential for the expression of captopril-induced increases in ethanol consumption.
Conclusions:
- The subfornical organ (SFO) plays a critical role in mediating the enhanced ethanol intake observed with chronic low-dose captopril treatment.
- Local angiotensin II synthesis and receptor activation within the SFO are likely mechanisms driving captopril-enhanced ethanol drinking.