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Strategies to Optimize the Antidepressant Action of Selective Serotonin Reuptake Inhibitors

  • Chapter
Antidepressants

Part of the book series: Contemporary Neuroscience ((CNEURO))

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Abstract

It is beyond doubt that major depression can be treated by selectively manipulating the function of different brain neurotransmitters (1,2). Yet, of the many brain neuronal systems, the serotonin (5-hydroxytryptamine, 5-HT) system is the most common neurobiological target for such treatments. Tricyclic antidepressants (TCAs) act on 5-HT and noradrenergic (NE) neurons by inhibiting, with different potencies, transmitter reuptake (3,4), and monoamine (MAO) oxidase inhibitors (MAOIs) increase 5-HT and NE transmission by preventing their metabolism. Yet, it was not until the advent of the selective serotonin reuptake inhibitors (SSRIs) that the antidepressant potential of 5-HT transporter blockade was fully appreciated (5,6). The clinically useful SSRIs are chemically dissimilar, but share the property of selectively inhibiting the 5-HT reuptake process (Fig. 1) Unlike TCAs, the SSRIs display little affinity for aminergic receptors (7) and therefore lack the severe side effects associated with the use of the former agents. This results in both an improved quality of life for the patients and greater treatment compliance, which is compromised in some instances by the use of TCAs. It is generally recognized that the antidepressant efficacy of SSRIs is comparable to that of TCAs, although several studies have shown that the latter are more effective in severely depressed inpatients (5,6,8,9).

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Romero, L., Casanovas, J.M., Hervás, I., Cortés, R., Artigas, F. (1997). Strategies to Optimize the Antidepressant Action of Selective Serotonin Reuptake Inhibitors. In: Skolnick, P. (eds) Antidepressants. Contemporary Neuroscience. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-474-0_1

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