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Pertussis toxin attenuates intracranial morphine self-administration
1Department of Pharmacology, College of Medicine, University of California, Irvine 92717.
Pharmacology, Biochemistry, and Behavior
|November 1, 1993
Summary
Pertussis toxin (PTX) blocks opioid reinforcement by inactivating inhibitory G-proteins in the hippocampus and ventral tegmental area (VTA). This selective action highlights the role of these G-proteins in mediating the rewarding effects of opioids.
Area of Science:
- Neuroscience
- Pharmacology
- Molecular Biology
Background:
- Mu and delta opioid receptors are key in mediating the rewarding effects of opioids.
- These receptors signal through pertussis toxin (PTX)-sensitive inhibitory G-proteins.
Purpose of the Study:
- To investigate if PTX can block opioid reinforcement signals.
- To determine the role of inhibitory G-proteins in mediating opioid reinforcement in specific brain regions.
Main Methods:
- Rats received intrahippocampal or intraventral tegmental area (VTA) injections of morphine.
- Pretreatment with PTX was administered in the hippocampus or VTA.
- Morphine self-administration and food-pellet reinforced behavior were assessed.
Main Results:
- Hippocampal PTX pretreatment blocked the acquisition of morphine self-administration.
- VTA PTX injections abolished morphine self-administration but not food-reinforced behavior.
- Inactivated PTX did not affect VTA morphine self-administration, confirming PTX's specific mechanism.
Conclusions:
- Inhibitory G-proteins in the hippocampus and VTA are crucial for mediating opioid reinforcement.
- PTX selectively blocks opioid reinforcement by enzymatically inactivating these G-proteins.
- These findings support the hypothesis that G-protein signaling pathways are essential for opioid drug reward.