Abstract
Antidepressant drugs have been used clinically not only for depression but also for other psychiatric disorders. Despite extensive studies, the mechanisms of action of antidepressant drugs have not been clearly established. The classic monoamine hypothesis of depression suggests that depressive disorders are associated with subnormal monoamine release at certain synapses of the CNS. Antidepressant drugs are supposed to increase the availability of noradrenaline and serotonin, either by inhibiting amine reuptake or by blocking monoamine oxidase in presynaptic nerve terminals, and facilitate monoamine transmission (Schildkraut 1965). However, an acute effect of antidepressants on neurotransmission is inconsistent with the delayed onset of clinical efficacy of these drugs (Zemlan and Garver 1990). Furthermore, neuroleptic drugs such as amphetamine and cocaine that block reuptake or catabolism of monoamines do not have an antidepressant effect. Thus, an acute neurochemical effect of antidepressant drugs may not account for the mechanism of action of these drugs.
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Hatta, S., Ohshika, H. (1998). Participation of Cytoskeletal Elements in Neuronal Signal Transduction: New Insight into the Molecular Basis of Antidepressant Action. In: Ozawa, H., Saito, T., Takahata, N. (eds) Signal Transduction in Affective Disorders. Springer, Tokyo. https://doi.org/10.1007/978-4-431-68479-4_9
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DOI: https://doi.org/10.1007/978-4-431-68479-4_9
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