Alpha 2-adrenoceptor responsivity in depression: effect of chronic treatment with moclobemide, a selective MAO-A-inhibitor, versus maprotiline.

Abstract

The effect of chronic treatment with the selective and reversible MAO-A-inhibitor moclobemide (MOC) vs. the norepinephrine reuptake inhibitor maprotiline (MAP) on alpha 2-adrenoceptor responsivity was studied by clonidine (CLON)-evoked growth hormone (GH) release in major depressive disorder. Compared to matched controls the depressed patients showed attenuated CLON-induced GH responses before treatment with MOC or MAP. Chronic treatment with both MOC and MAP significantly improved the depressive symptomatology. Although a trend toward increased GH responses to CLON was demonstrated after treatment in both groups, neither MOC nor MAP had a complete effect on restoration of alpha 2-adrenoceptor responsivity. No difference in insulin-like growth factor I (IGF-I) plasma concentrations before and after treatment with MOC or MAP was found. Our results support the view that antidepressants with different mechanisms of action may be capable of restoring alpha 2-adrenoceptor function during recovery from a major depressive episode.