Multiple Hormone Responses to Stimulation with dl-Fenfluramine in Patients with Major Depression before and after Antidepressive Treatment

Kasper, S.; Vieira, Ana Beatriz Duarte; Schmidt, Roland; Richter, Petra

doi:10.1055/s-2007-1014487

Cited by 32 publications

(20 citation statements)

References 12 publications

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“…In patients chronically treated with SSRIs, a normalization of the blunted PRL response would be expected. However, results have been conflicting with some studies showing enhanced PRL response (Kasper et al, 1990;O'Keane et al, 1992), and others finding no change or even decrements in the response (Dulchin et al, 2001;Kavoussi et al, 1999). These studies underscore how individual differences in serotonin responsivity are reflected in variable PRL responsivity across patient samples.…”

Section: The Ssris and Prolactinmentioning

confidence: 93%

From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

Emiliano

Fudge

2004

Neuropsychopharmacol

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The widespread use of the selective serotonin reuptake inhibitors (SSRIs) has been accompanied by numerous reports describing a potential association with hyperprolactinemia. Antipsychotics are commonly known to elevate serum prolactin (PRL) through blockade of dopamine receptors in the pituitary. However, there is little awareness of the mechanisms by which SSRIs stimulate PRL release. Hyperprolactinemia may result in overt symptoms such as galactorrhea, which may be accompanied by impaired fertility. Long-term clinical sequelae include decreased bone density and the possibility of an increased risk of breast cancer. Through literature review, we explore the possible pathways involved in serotonin-induced PRL release. While the classic mechanism of antipsychotic-induced hyperprolactinemia directly involves dopamine cells in the tuberoinfundibular pathway, SSRIs may act on this system indirectly through GABAergic neurons. Alternate pathways involve serotonin stimulation of vasoactive intestinal peptide (VIP) and oxytocin (OT) release. We conclude with a comprehensive review of clinical sequelae associated with hyperprolactinemia, and the potential role of SSRIs in this phenomenon.

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Section: The Ssris and Prolactinmentioning

confidence: 93%

From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

Emiliano

Fudge

2004

Neuropsychopharmacol

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“…Studies that compare prolactin response to fenfluramine in depressed patients before and after antidepressant treatment have yielded mixed results. [344][345][346] Citalopram is a highly selective 5-HT reuptake inhibitor that produces dose-related increases in prolactin and cortisol in normal subjects. 347,348 Intravenous challenge with citalopram has been reported to result in a blunted prolactin response in depressed patients compared to healthy controls, 3,334 while cortisol secretion was reported not to differ between groups.…”

Section: Experimental Manipulations Of 5-ht In Relation To Sv Factorsmentioning

confidence: 99%

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

et al. 2006

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In recent years, the term serotonergic vulnerability (SV) has been used in scientific literature, but so far it has not been explicitly defined. This review article attempts to elucidate the SV concept. SV can be defined as increased sensitivity to natural or experimental alterations of the serotonergic (5-HTergic) system. Several factors that may disrupt the 5-HTergic system and hence contribute to SV are discussed, including genetic factors, female gender, personality characteristics, several types of stress and drug use. It is explained that SV can be demonstrated by means of manipulations of the 5-HTergic system, such as 5-HT challenges or acute tryptophan depletion (ATD). Results of 5-HT challenge studies and ATD studies are discussed in terms of their implications for the concept of SV. A model is proposed in which a combination of various factors that may compromise 5-HT functioning in one person can result in depression or other 5-HT-related pathology. By manipulating 5-HT levels, in particular with ATD, vulnerable subjects may be identified before pathology initiates, providing the opportunity to take preventive action. Although it is not likely that this model applies to all cases of depression, or is able to identify all vulnerable subjects, the strength of the model is that it may enable identification of vulnerable subjects before the 5-HT related pathology occurs. Molecular Psychiatry ( Keywords: serotonin; mood disorders; stress; genetics; sex; tryptophan Involvement of serotonin in depressionMood disorders are one of the most prevalent forms of mental illness. 1 According to the DSM-IV, the lifetime risk for major depressive disorder is between 10 and 25% for women and between 5 and 12% for men. 2 Depression has been studied intensively during the last few decades, but the psychological and neurobiological determinants of depression have not yet been precisely defined. Although several factors are known to contribute to the etiology of depression, it is not clear how these factors cause depression, and why some subjects become depressed while others remain unaffected. In terms of biological factors in the etiology of depression, there are several hypotheses. These include neurotransmitter dysfunctions (serotonin, 5-HT; dopamine, DA; norepinephrine, NE); dysregulations in hypothalamic-pituitary-adrenal (HPA) axis activity; and immune system imbalance. The aim of this article is not to discuss all of these hypotheses in detail, but to evaluate the role that serotonin may play within these hypothesized mechanisms.It is widely accepted that diminished serotonergic (5-HTergic) function is involved in the onset and course of depression. 3,4 The 5-HTergic system is a large and complex system. Although nearly all cell bodies of 5-HTergic neurons are located in the raphe nuclei in the brain stem, the axons of these neurons innervate almost the entire brain. The actions of 5-HT are mediated by 16 types and subtypes of receptors. 5 As the 5-HTergic system is assumed to be a modulatory system, the exact func...

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“…Disturbed serotonin function in Major Depression has been evident from in vivo challenge studies of serotonin responsivity using clomipramine (Leatherman et al 1993), tryptophan (Charney et al 1984), ipsapirone (Lesch 1991), m-chlorphenylpiperazine (mCPP) (Quested et al 1997), 1-5 hydroxytryptophan (Maes and Meltzer 1995), and fenfluramine (Mann et al 1995Siever et al 1984;Shapira et al 1993Shapira et al , 1992aKasper et al 1990;Flory et al 1998;Malone et al 1996;Mokrani et al 1997).…”

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confidence: 99%