Basal Prolactin Values Correlate with Response to Reboxetine Treatment in Major Depression, but Not with Response to Citalopram

Abstract

Little is known about variables that might predict outcome in major depression. Recently, basal prolactin values (BPV) have been suggested to predict response to treatment with tricyclic antidepressive drugs. In order to examine whether BPV predict response to selective mono-aminergic therapy, 24 in-patients with major depression were treated in a single-masked, randomised study using the most selective noradrenergic or serotonergic reuptake inhibitors available for antidepressant treatment, i.e. reboxetine and citalopram. A significant correlation between BPV and treatment response to reboxetine was found, but not between BPV and response to citalopram. As BPV are influenced by noradrenergic activity, it can be hypothesized that depressed patients with comparatively high BPV have a relatively high noradrenergic function. This might explain why in our study depressed patients with the highest BPV responded strongest to selective noradrenergic treatment with reboxetine. As measurement of BPV is simple, further studies are suggested to examine the possible clinical value of the link between prolactin, noradrenergic function in major depression and treatment response.

Strain differences in the distribution of dopamine (DA-2 and DA-3) receptor sites in rat brain

“…One explanation may be that DA levels are higher in these brain areas and may lead to hypoprolactinemia, which has been associated with depressive behavior (Moeller et al, 2005).…”

Reboxetine may cause amenorrhea in female patients

“…Moreover, basal prolactin levels have been reported to be predictive for response to reboxetine treatment in major depression, but not for response to citalopram [5]. It has also been reported that antidepressants which selectively modify noradrenergic function also have effects on serotonin function, as measured by neuroendocrine testing, since after 6 weeks of treatment they increase serotonin-mediated cortisol response to D-fenfluramine, a specific 5-HT releasing agent without the catecholamine effects [6].…”

Wie wirken Antidepressiva? Weil sie einen Serotoninmangel im Gehirn ausgleichen?

“…Zum einen ist sowohl die selektive Rückaufnahme von Serotonin [20][21][22] wie auch von Noradrenalin [22,23] antidepressiv wirksam: Auch wenn im Einzelnen Serotonin und Noradrenalin zu differentiellen Effekten im Zentralnervensystem (ZNS) führen [24][25][26], ist die antidepressive Wirksamkeitalsonichtexklusiv mit einem einzelnen Monoamin verknüpft.…”