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Cholecystokinin and satiation with alcohol
P J Kulkosky1, M R Sanchez, M A Foderaro
1Department of Psychology, University of Southern Colorado, Pueblo 81001-4901.
Alcohol (Fayetteville, N.Y.)
|September 1, 1989
Summary
Cholecystokinin (CCK) administration suppresses alcohol intake in rats, acting as a satiety signal. This effect is time-limited and requires prior alcohol experience, suggesting a conditioned response.
Area of Science:
- Neuroscience
- Gastroenterology
- Behavioral Science
Background:
- The brain-gut peptide cholecystokinin (CCK) is released by ethanol in the stomach.
- Peripheral CCK administration has been shown to reduce ethanol consumption.
Purpose of the Study:
- To investigate the temporal and motivational specificity of CCK's inhibitory effects on alcohol intake.
- To explore the role of CCK as a potential preabsorptive satiety signal for ethanol.
Main Methods:
- Rats were administered CCK octapeptide intraperitoneally followed by access to ethanol at varying time points.
- Two-bottle choice tests (ethanol vs. water) were used to assess motivational specificity.
- Interactions between CCK and naloxone (opioid receptor blocker) were examined.
Main Results:
- CCK's inhibitory effect on ethanol intake was significant only when ethanol access was delayed by 20 minutes.
- CCK specifically suppressed ethanol solution intake without affecting water intake.
- The inhibitory effect of CCK on ethanol consumption required prior ethanol experience and involved opioid receptor-mediated processes.
Conclusions:
- CCK acts as a satiety signal for ethanol, with its effect being temporally constrained and motivationally specific.
- The satiety action of CCK appears to be conditioned, relying on the expectancy of alcohol's postingestive effects.
- CCK may interact with endogenous opioid systems to mediate ethanol intake inhibition.