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Glucocorticoid interactions with ethanol effects on synaptic plasma membranes: influence on [125I]calmodulin binding
1Department of Pharmacology and Molecular Biology, Chicago Medical School, Illinois, USA.
The Journal of Pharmacology and Experimental Therapeutics
|February 1, 1996
Summary
Glucocorticoids can counteract ethanol's effects on brain calmodulin (CaM) binding. This steroid specificity suggests endogenous factors modulate neuronal sensitivity to alcohol.
Area of Science:
- Neuroscience
- Neurochemistry
- Pharmacology
Background:
- Ethanol inhibits calmodulin (CaM) binding to brain synaptic membranes.
- Glucocorticoids stimulate CaM binding, opposing ethanol's effects.
- This suggests a potential interaction relevant to ethanol sensitivity.
Purpose of the Study:
- To characterize corticosterone's interaction with ethanol's effects on [125I]CaM binding.
- To investigate the neurochemical basis of glucocorticoid antagonism of ethanol's effects.
Main Methods:
- In vitro study using brain synaptic plasma membranes.
- Analysis of [125I]CaM binding in the presence of ethanol and corticosterone.
- Concentration-response curves and Scatchard analyses were performed.
Main Results:
- Ethanol and corticosterone exhibited an additive interaction on [125I]CaM binding.
- Ethanol decreased membrane affinity for CaM; corticosterone antagonized this effect.
- Glucocorticoids (cortisol, dexamethasone, triamcinolone) were effective, while gonadal steroids were not.
Conclusions:
- Glucocorticoids antagonize ethanol's inhibition of CaM binding.
- The interaction involves alterations in membrane affinity for CaM.
- These findings support the role of glucocorticoids in modulating neuronal ethanol sensitivity.