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Antidepressants drugs (ADS) have traditionally been assumed to exert their therapeutic effect by increasing noradrenergic and/or serotoninergic transmission. Tricyclic ADS block the reuptake of noradrenaline and/or serotonin, MA0 inhibitors prevent the enzymatic degradation of monoamines. Either mechanism results in an increase of monoamine concentration in the synaptic cleft (Baldessarini, 1985).

However, the clinical response to these drugs occurs only after 2-3 weeks of treatment, while reuptake and MA0 inhibition are produced immediately after single doses of these compounds (Baldessarini, 1985). Moreover, some clinically effective ADS, namely Mianserin and Iprindole, do not inhibit the amine uptake or MA0 (Zis and Goodwin, 1979). These observations have led numerous authors to question the classical hypothesis on the mechanism of action of ADS and to perform studies on the effects of chronic …