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Chronic morphine administration augments benzodiazepine binding and GABAA receptor function.
F Lopez1, L G Miller, M L Thompson
1Department of Psychiatry, Tufts University School of Medicine, Boston, MA.
Psychopharmacology
|January 1, 1990
Summary
Chronic morphine enhances GABAA receptor function and benzodiazepine binding in mice, suggesting opioid receptor involvement. Naltrexone reversed these effects, indicating the opioid system
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Behavioral and neurochemical studies suggest interactions between opioid and GABA neurotransmitter systems.
- The GABAA receptor is a primary site for postsynaptic GABAergic activity.
Purpose of the Study:
- To investigate the impact of chronic opiate administration on GABAA receptor function.
- To assess the effects of chronic morphine and naltrexone on benzodiazepine and TBPS binding and GABA-dependent chloride uptake.
Main Methods:
- Mice were administered chronic morphine or naltrexone.
- Evaluated binding at benzodiazepine and t-butylbicyclophosphorothionate (TBPS) sites.
- Measured GABA-dependent chloride uptake.
Main Results:
- Chronic morphine increased in vivo benzodiazepine receptor binding in the cortex.
- Muscimol-stimulated chloride uptake increased at low doses after chronic morphine.
- Naltrexone administration did not alter binding or uptake, but reversed morphine-induced changes.
Conclusions:
- Chronic morphine enhances benzodiazepine binding and GABAA receptor function, potentially via opioid receptors.
- Naltrexone blocks these effects, confirming the role of opioid receptor activation.
- These findings elucidate the neurochemical interplay between opioid and GABA systems.