Both ethanol and desipramine influence β-adrenoceptor regulation. We reported previously that ethanol partially counteracted desipramine's effects on β-adrenoceptor. Previous studies utilized β-adrenoceptor radioligands that also bind to 5-HT(1B) receptors, thus, changes in 5-HT(1B) receptors could have confounded the results. The effects of chronic ethanol, desipramine and ethanol/desipramine treatment on β-adrenoceptor coupling efficiency to G(s) protein in rat brain were examined using 125I-iodocyanopindolol after blocking binding to 5-HT(1B) receptors. In the frontal cortex, ethanol uncoupled β-adrenoceptor from G(s). Desipramine decreased β-adrenoceptor density, particularly in the high-conformational state, with no effect on coupling. In combined treatment, desipramine prevented ethanol-induced uncoupling. In the hippocampus, desipramine enhanced β-adrenoceptor coupling, but ethanol had no effect. In combination with desipramine, ethanol enhanced desipramine-induced decrease in β-adrenoceptor density in the high-conformational state, but uncoupled β-adrenoceptors, an effect not observed with ethanol alone. These results suggest a complex interplay between ethanol and antidepressants in modulating β-adrenoceptor function. Copyright (C) 1998 Elsevier Science B.V.
- G(s) protein
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