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Hypercortisolism in depression has been extensively studied during the last three decades. The main hypothesis regarding origin and clinical relevance of this phenomenon, however, has changed significantly. Up to the mid-seventies hypercortisolism was conceived as consequence of stress modified by the degree of unconscious defense mechanisms in different forms of depressive or non-depressive psychiatric disorders. At the end of the seventies this point of view changed considerably. Hypercortisolism was regarded as a biological statemarker of the endogenous subtype of depression with clinical differential-diagnostic relevance. An abnormal dexamethasone suppression test (DST) was assumed to be the best indication of increased activation of the cortisol system. These conslusions turned out to be wrong. DSTresults are not specific for melancholia and the test seems to be of limited value for measuring the function of the HPA-axis. Intervening variables, such as weight loss, drug and alcohol withdrawal or situational stress, influence the test results significantly, independent of the nosological classification. Additionally, interindividual differences in the susceptibility of the HPA-axis may decisively influence the activation of the HPA-axis as well in healthy subjects under stress as in psychiatric patients.

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The hypothesis of a significant involvement of the cholinergic system in the pathogenesis of affective disorders still lacks strong experimental support. This is mainly because of missing specific peripheral markers of the central nervous activity of the cholinergic system and the lack of specific cholinergic agonists and antagonists without severe peripheral side effects. As the direct cholinergic agonist RS 86 seems to be more suitable because of its minor side effects, long half‐life and oral applicability, it was tested for its antimanic property and its effect on the hypothalamo‐pituitary adrenal system and the rapid eye movement (REM) sleep‐generating system. RS 86 exhibited antimanic and REM sleep‐inducing properties, but failed to stimulate the Cortisol system.