Prolactin secretion in man: a useful tool to evaluate the activity of drugs on central 5‐hydroxytryptaminergic neurones. Studies with fenfluramine.

Quattrone, Aldo; Tedeschi, G; Aguglia, Umberto; Scopacasa, Francesco; Direnzo, GF; Annunziato, Lucio

doi:10.1111/j.1365-2125.1983.tb02202.x

Cited by 157 publications

(50 citation statements)

References 19 publications

(17 reference statements)

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“…These effects are similar to the effects of 8-0H-DPAT (the prototypical 5-HT 1a receptor agonist) in rats (Gilbert et al 1988;Aulakh et al 1988). Buspirone also increases serum prolactin in both laboratory animals and man (Meltzer et al 1982(Meltzer et al , 1983Cowen et al 1990), similar to the 5-HT -releasing agent fenfluramine (Serri et al 1987;Coccaro et al 1988;Siever et al 1984;Quattrone et al 1983), and the 5-HT precursors L-tryptophan and 5-HTP (Lamberts et al (1978;MacIndoe et al 1973).…”

Section: Resultsmentioning

confidence: 90%

A Preliminary Neuroendocrine Study with Buspirone in Major Depression

Moeller

Steinberg

Fulton

et al. 1994

Neuropsychopharmacol

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We administered the serotonin-1a agonist buspirone (0.4 mglkg orally) as a neuroendocrine challenge agent to a group of male patients with DSM-III -R major depressive disorder (MOD) (n = 13) and a group of male healthy controls (n = 10). The primary hypothesis of the study was that the prolactin response to buspirone would be blunted in the depressed patients. The prolactin response was significantly lower in depressed patients than in controls. There was no significant relationship between KEY WORDS: Depressive disorder; Serotonin; Buspirone; Prolactin 655 Avenue of the Americas, New York, NY 10010 placebo corrected-peak prolactin level and severity of depression or suicidality. There was a nonsignificant trend for the melancholic (n = 5) depressed patients to have a lower placebo corrected-peak prolactin level than nonmelancholic depressed patients (n = B).Our findings support a role for the serotonin-1a receptor in the etiology of MOD, specifically at the postsynaptic site. and 5-HT -releasing agents (Siever et al. 1984; Coccaro et al. 1989;Mitchell and Smythe 1990;Lichtenberg et al. 1992;Shapira et al. 1992aShapira et al. , 1992b.There has been a relatively consistent ii.nding of de creased prolactin response to various serotonergic agents in subjects with major depressive disorder (MOD) using nonspecific 5-HT challenge agents; thus, recent research has focused on the role of specific subtypes

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Section: Resultsmentioning

confidence: 90%

A Preliminary Neuroendocrine Study with Buspirone in Major Depression

Moeller

Steinberg

Fulton

et al. 1994

Neuropsychopharmacol

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“…On the other hand, even in psychiatric groups at the highest risk, most patients never attempt suicide, thus suggesting that the predisposition to demonstrate suicidal behavior is independent of the main psychiatric disorders. Alterations of the serotonergic system have been repeatedly reported in suicide victims, such as the reduced concentration of 5-hydroxyindolacetic acid in the cerebrospinal fluid or the blunted prolactin response to fenfluramine, and seem to be independent of the psychiatric diagnoses and correlate with the lethality of suicide attempts (Asberg et al, 1976;Quattrone et al, 1983). Kety (1986) suggested that one of the major genetic factors in suicide may be related to an inability to control impulsive behavior in psychiatric and psychogenic conditions.…”

Section: Discussionmentioning

confidence: 99%

Association of RGS2 Gene Polymorphisms with Suicide and Increased RGS2 Immunoreactivity in the Postmortem Brain of Suicide Victims

Cui

Nishiguchi

Ivleva

et al. 2007

Neuropsychopharmacol

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Regulators of G-protein signaling are a family of proteins that negatively regulate the intracellular signaling of G protein-coupled receptors, such as the serotonin receptor. Recent studies have suggested that one of these proteins, the regulator of G-protein signaling 2 (RGS2), plays an important part in anxiety and/or aggressive behavior. To explore the involvement of the RGS2 gene in the vulnerability to suicide, we screened Japanese suicide victims for sequence variations in the RGS2 gene and carried out an association study of RGS2 gene polymorphisms with suicide victims. In the eight identified polymorphisms that were identified by mutation screening, we genotyped four common single-nucleotide polymorphisms (SNPs) in the RGS2 gene, and found significant differences in the distribution of the SNP3 (C + 2971G, rs4606) genotypes and alleles of the SNP2 (C-395G, rs2746072) and the SNP3 between completed suicides and the controls. The distribution of the haplotype was also significantly different between the two groups (global po0.0001). Furthermore, RGS2 immunoreactivity significantly increased in the amygdala and the prefrontal cortex (Brodmann area 9 (BA9)) of the postmortem brain of the suicide subjects. These findings suggest that RGS2 is genetically involved in the biological susceptibility to suicide in the Japanese population.

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“…[337][338][339] Administration of D-fenfluramine results in a dosedependent rise in prolactin levels, 340 which has been used as an index of central 5-HT responsivity. [341][342][343] The prolactin response to fenfluramine in depression has been studied extensively, with mixed results (for review see Kavoussi et al 340 ). Studies that compare prolactin response to fenfluramine in depressed patients before and after antidepressant treatment have yielded mixed results.…”

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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Prolactin secretion in man: a useful tool to evaluate the activity of drugs on central 5‐hydroxytryptaminergic neurones. Studies with fenfluramine.

Cited by 157 publications

References 19 publications

A Preliminary Neuroendocrine Study with Buspirone in Major Depression

A Preliminary Neuroendocrine Study with Buspirone in Major Depression

Association of RGS2 Gene Polymorphisms with Suicide and Increased RGS2 Immunoreactivity in the Postmortem Brain of Suicide Victims

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

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