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Morphine responsiveness and seizure proneness
Experimental Neurology
|August 1, 1984
Summary
Seizure proneness, induced by convulsions or brain damage, heightens morphine sensitivity. This effect, blocked by naltrexone after prior convulsions, may involve changes in opiate receptors.
Area of Science:
- Neuroscience
- Pharmacology
- Epilepsy Research
Background:
- Previous studies showed amygdala kindling increases morphine sensitivity and Straub tail response.
- These effects persisted for 3 months post-convulsion and were blocked by naloxone.
Purpose of the Study:
- To investigate if other seizure-inducing methods (metrazol, ECS) and brain damage affect morphine sensitivity.
- To determine if these enhanced responses are blocked by naltrexone.
- To explore the role of diurnal rhythms in morphine sensitivity after amygdala kindling.
Main Methods:
- Induction of convulsions using metrazol or electroshock (ECS) in animal models.
- Assessment of morphine's convulsive effects and Straub tail response.
- Induction of brain damage via electrode implantation or skull screw penetration.
- Administration of naltrexone to block opioid receptor activity.
- Evaluation of morphine sensitivity across diurnal cycles.
Main Results:
- Metrazol and ECS-induced convulsions enhanced morphine response, blocked by naltrexone.
- Brain damage alone increased morphine sensitivity, but this was not blocked by naltrexone.
- Amygdala-kindled animals showed heightened morphine sensitivity during their dark phase (higher opiate receptor activity).
Conclusions:
- Seizure proneness, from prior convulsions or brain damage, increases sensitivity to morphine.
- The opioid system is implicated, particularly when prior convulsions have occurred, suggesting potential opiate receptor alterations.