Abstract
The first antidepressant drug, isoniasid, was coincidentally discovered in 1953, when the aim was to develop new antituberculosis medication [1]. It was suggested that the antidepressant effect of isoniaside could be explained by its ability to inhibit monoamine oxidase (MAO), an enzyme metabolizing serotonin (5-HT), norepinephrine (NE) and dopamine (DA). It was therefore hypothesized that depression and affective disorders result from reduced transmission within 5-HT, NE and/or DA systems [2-4]. Based on this hypothesis, two first families of antidepressant drugs were developed. They are MAO inhibitors (like the abovementioned isoniasid) and tricyclic antidepressants (TCAs). MAO inhibitors increase 5-HT, NE and DA availability by suppressing their metabolism [5, 6]. TCAs stimulate monoamine tone by inhibiting the reuptake of 5-HT, NE and/or DA [7, 8].
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