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The effects of proglumide on morphine induced motility changes
Psychopharmacology
|January 1, 1984
Summary
Cholecystokinin (CCK) antagonists like proglumide potentiate morphine-induced hypokinesia in rats. This suggests endogenous CCK tonically opposes opiate effects on motility.
Area of Science:
- Neuropharmacology
- Gastroenterology
- Behavioral Science
Background:
- Cholecystokinin (CCK) is a peptide neurotransmitter implicated in various physiological processes, including pain modulation and gastrointestinal function.
- Opiates, such as morphine, are well-known for their analgesic properties and their effects on motor activity.
- The interaction between CCK and opioid systems is an area of ongoing research.
Purpose of the Study:
- To investigate the role of cholecystokinin (CCK) in modulating the effects of morphine on rat behavior.
- To determine if CCK antagonism influences morphine-induced hypokinesia (reduced motor activity).
Main Methods:
- Rats were administered proglumide, a CCK antagonist, at a dose of 0.02 mg/kg.
- Morphine was administered at varying doses (0, 5, 15, or 45 mg/kg) concurrently with or without proglumide.
- Behavioral activation and hypokinesia were assessed to evaluate the motor effects.
Main Results:
- Proglumide alone showed a trend towards increased behavioral activation in rats.
- Proglumide significantly potentiated the hypokinesia induced by morphine administration.
- These findings suggest a modulatory role for CCK in opioid-induced changes in motility.
Conclusions:
- Endogenous cholecystokinin (CCK) appears to tonically antagonize opioid modulation of motor activity.
- This antagonism is observed regardless of whether the opioid effects are mediated by endogenous or exogenous sources.
- CCK antagonists may alter the behavioral outcomes of opioid administration.