Neuroendocrine disorders in depressions and their significance for the monoamine hypothesis of depression

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Abstract
This article discusses the results of recent neuroendocrinological research in depressions. The abnormalities found in a given category of vital depressive patients--cortisol hypersecretion, decreased growth hormone response to insulin hypoglycaemia and decreased luteinizing hormone secretion in menopause--are believed to be due to deficient noradrenalin-(NA)-ergic activity in the hypothalmus. Thus explained, they support the so-called MA (monoamine) hypothesis, which postulates that a functional NA deficiency in the brain plays a role in the pathogenesis of certain types of vital depression. Disorders in certain central MA-ergic systems are predictive of disorders in the hormone secretion of the anterior pituitary. Inversely, disorders in the hormone secretion of the anterior pituitary can be indicative of disorders in the MA-ergic transmission in the hypothalamus. Consequently we can expect a convergence of transmitter research and neuroendocrinological research--two lines of research which have so far been largely separated in studies of human individuals.