Abstract
The noradrenergic control of melatonin secretion in rat and man appears to have the property of a typical central noradrenergic system. Using the pineal as a model, increases and decreases in plasma melatonin levels are used to monitor the respective changes in noradrenergic transmission. Although in rats chronic imipramine treatment reduced pineal adrenoreceptor binding sites and melatonin levels, in depressed patients chronic treatment with desimipramine results in increases in plasma melatonin levels. These data support the classical view that in man antidepressants act by increasing monoamine transmission. The author postulates in depression a primary lesion distal to the monoaminergic projections but proximal to the hypothalamic nuclei, and further, that antidepressants may have a common effect on an as yet unidentified, hypothalamic neuropeptide.

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