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Dexamethasone reduced clonidine-induced hypoactivity in mice
A Capasso1, A Di Giannuario, A Loizzo
1School of Pharmacy, University of Salerno, Italy.
The Journal of Pharmacy and Pharmacology
|June 1, 1996
Summary
Dexamethasone pretreatment reduces clonidine-induced locomotor hypoactivity in mice. This effect involves protein synthesis mediated by the glucocorticoid receptor in the brain.
Area of Science:
- Neuropharmacology
- Endocrinology
Background:
- Clonidine induces anti-nociception and locomotor hypoactivity in mice.
- Dexamethasone's effect on clonidine-induced anti-nociception suggests interaction with central nervous system pathways.
Purpose of the Study:
- To investigate the effect of dexamethasone pretreatment on clonidine-induced locomotor hypoactivity in mice.
- To elucidate the underlying mechanisms of dexamethasone's modulatory action on clonidine-induced behaviors.
Main Methods:
- Mice were pretreated with varying doses of dexamethasone (intraperitoneally or centrally) before clonidine administration.
- Locomotor activity was measured using an activity cage.
- The role of protein synthesis and glucocorticoid receptors was assessed using cycloheximide and RU38486, respectively.
Main Results:
- Dexamethasone dose-dependently reduced clonidine-induced locomotor hypoactivity.
- Central administration of dexamethasone also attenuated this effect.
- Cycloheximide blocked dexamethasone's effect, while RU38486 antagonized it, indicating involvement of protein synthesis and glucocorticoid receptors.
Conclusions:
- Dexamethasone modulates clonidine-induced locomotor hypoactivity through a mechanism involving protein synthesis.
- Glucocorticoid receptor activation in the brain is crucial for dexamethasone's observed effects.
- These findings highlight the complex interplay between glucocorticoids and adrenergic systems in regulating behavior.