Abstract
Changes in serotonergic (5HT) neurotransmission may mediate the therapeutic actions of some antidepressant drugs. In the present study, the 5HT precursor L-trytophan (L-TRP) was administered intravenously to nine depressed patients before and during treatment with the triazolopyridine anti-depressant trazodone (TRZ). Neuroendocrine, subjective mood, and cardiovascular responses to L-TRP were assessed. Unlike tricyclic antidepressants and monoamine oxidase inhibitors, TRZ did not enhance the prolactin response to L-TRP and had little effect on other measures. Since other studies indicate that the TRP-induced increase of prolactin in humans may reflect 5HT function, the present study suggests that TRZ treatment does not enhance net 5HT function in depressed patients.
Published Version
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