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Opiate induced feeding is not dependent on the hippocampus
Physiology & Behavior
|July 1, 1984
Summary
Opioid-induced feeding is not primarily mediated by the hippocampus. Studies show hippocampal lesions do not alter the feeding effects of opioid antagonists or agonists, suggesting other brain regions are involved.
Area of Science:
- Neuroscience
- Neuropharmacology
- Behavioral Neuroscience
Background:
- Spreading depression in the hippocampus can trigger feeding behavior.
- Opioid peptides are known to induce spreading depression when administered to the hippocampus.
Purpose of the Study:
- To investigate if spreading depression in the hippocampus is the main mechanism behind opioid-induced feeding.
- To determine the role of the hippocampus in mediating the feeding effects of opiates.
Main Methods:
- Tested the feeding effects of naloxone (opiate antagonist) and butorphanol tartrate (kappa-sigma agonist) in rats.
- Compared the effects in rats with hippocampal lesions versus control (sham) rats.
Main Results:
- Naloxone reduced food intake similarly in both lesioned and sham rats.
- Butorphanol tartrate increased food intake equally in both lesioned and sham rats.
Conclusions:
- The hippocampus is not the primary brain structure responsible for opioid-induced feeding.
- These findings suggest that other neural pathways mediate the effects of opiates on appetite.