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Francesc Artigas, PhD; Victor Perez, MD; Enric Alvarez, MD
Department of Neurochemistry, CID, CSIC Department of Psychiatry Hospital de Sant Pau Centre d'Investigació i Desenvolupament, CSIC Jordi Girona 18-26 08034 Barcelona, Spain

Arch Gen Psychiatry. 1994;51(3):248-251.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Preclinical evidence indicates that repeated treatment with antidepressant drugs (serotonin [5-HT] reuptake or monoamine oxidase [MAO] inhibitors) potentiates the ascending brain serotonergic pathways.^1,2 Also, clinical data show that the inhibition of 5-HT synthesis results in a marked worsening of patients recovering from depression who are treated with these drugs.^3-5 These findings suggest that the antidepressant effects of uptake and MAO inhibitors emerge when serotonergic activity increases.

Using intracerebral microdialysis in the awake, freely moving rat, a single treatment with 5-HT uptake blockers, such as clomipramine⁶ or fluvoxamine,⁷ was reported to cause little or no increase of 5-HT concentration in frontal cortex at doses comparable with or higher than those used clinically. In contrast, extracellular 5-HT concentration is dramatically augmented by the same doses in the vicinity of cell bodies of serotonergic neurons, in the midbrain raphe nuclei, a preferential increase also observed after a single treatment . . . [Full Text PDF of this Article]

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