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Repeated electroconvulsive shock attenuates clonidine-induced hypoactivity in rodents
European Journal of Pharmacology
|November 5, 1981
Summary
Repeated electroconvulsive shock (ECS) treatment reduces the hypoactivity caused by clonidine in rodents, suggesting it desensitizes brain alpha 2-adrenoceptors. This effect may indicate presynaptic receptor involvement.
Area of Science:
- Neuropharmacology
- Behavioral Neuroscience
Background:
- Clonidine, a low-dose stimulant of alpha 2-adrenoceptors, induces hypoactivity in rats and mice.
- This clonidine-induced hypoactivity is antagonized by yohimbine but not prazosin, indicating alpha 2-adrenoceptor mediation.
Purpose of the Study:
- To investigate the effect of repeated electroconvulsive shock (ECS) on clonidine-induced hypoactivity.
- To explore the potential role of alpha 2-adrenoceptor subsensitivity following repeated ECS.
Main Methods:
- Rodents (rats and mice) received daily electroconvulsive shock (ECS) for 10 days.
- Clonidine-induced hypoactivity was assessed 24 hours after the final ECS.
- Brain MOPEG-SO4 concentrations were measured in rats.
Main Results:
- Repeated daily ECS significantly attenuated clonidine-induced hypoactivity in both rats and mice.
- This attenuation was not observed after a single ECS or subconvulsive ECS.
- Repeated ECS abolished the decrease in rat brain MOPEG-SO4 concentrations induced by clonidine.
Conclusions:
- Repeated ECS induces a subsensitivity of alpha 2-adrenoceptors in the brain.
- These findings suggest that alpha 2-adrenoceptors, potentially located presynaptically, are involved in the hypoactive effects of clonidine and are modulated by repeated ECS.