Abstract
The development of antidepressants and of theories as to the causes of depression have taken a parallel course and have influenced each other. All classic antidepressants have the property of potentiating monoaminergic transmission, either by inhibiting neuronal reuptake or by inhibiting the monoamino-oxidase enzymes. To explain the clinical efficacy of these drugs, it was assumed in the theories about depression that the disease is induced by a deficiency of noradrenaline (NA), serotonin, or dopamine at the neuronal-synaptic receptor sites (Bunney and Davis 1965; Lapin and Oxenkrug 1969; Randrup and Braestrup 1977). Research was therefore carried out to discover antidepressants which selectively potentiate noradrenergic, serotoninergic, or dopaminergic transmission. There is now no doubt about the therapeutic efficacy of selective inhibitors of NA reuptake (such as maprotiline), but that of the selective inhibitors of serotonin reuptake (such as zimelidine and fluoxetine) is still disputed.
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Wendt, G. (1990). Levoprotiline: Clinical Therapeutic Efficacy and Tolerability. In: Bunney, W.E., Hippius, H., Laakmann, G., Schmauss, M. (eds) Neuropsychopharmacology. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-74034-3_29
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DOI: https://doi.org/10.1007/978-3-642-74034-3_29
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