Abstract
The role of antidepressants in bringing about adaptive changes in peripheral and central neurotransmitter receptors is briefly reviewed and extended to show how changes in platelet and lymphocyte adrenoceptor and serotonin receptor activity may correlate with the depressed state and normalise following effective treatment. By contrast, the 3H-imipramine binding sites on the platelet membrane do not change following successful treatment and may therefore reflect a trait-dependent (genetic) change. The neuroendocrine markers, such as the dexamethasone suppression test (DST), have the advantage over the receptor markers in that they require less sophisticated laboratory facilities. It is concluded that a better insight into the aetiology and progress of depression may be gained by combining receptor markers with such neuroendocrine markers as the DST.