The Effect of Buspirone on Prolactin and Growth Hormone Secretion in Man

Meltzer, Herbert Y.; Flemming, Rachel; Robertson, Alan

doi:10.1001/archpsyc.1983.01790090061009

Cited by 92 publications

(39 citation statements)

References 33 publications

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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%

“…The second study by the same group found a blunted ipsapirone induced adrenocorticotrophic hormone (ACTH) re sponse in patients with MOD compared to controls (Lesch et al 1991). Both of these studies are interest ing; however, the results of these studies are difficult to interpret in light of the fact that the hypothermic re sponse may be a presynaptic autoreceptor response (Lesch et al 1991), and the ACTH response is thought to be postsynaptic (Meltzer et al 1983). …”

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confidence: 99%

“…Blood drawing was repeated at 15-minute intervals from 10:45 AM till 1:00 PM. The sched ule for blood drawing included the period of increase in neuroendocrine parameters in previous studies (Meltzer et al 1983). Approximately 10 cc of blood was drawn at each time point.…”

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confidence: 99%

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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%

mentioning

confidence: 99%

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A Preliminary Neuroendocrine Study with Buspirone in Major Depression

Moeller

Steinberg

Fulton

et al. 1994

Neuropsychopharmacol

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“…326,327 Neuroendocrine responses to 5-HT agonists are an indication of postsynaptic receptor sensitivity, with relatively high hormonal responses being indicative of receptor hypersensitivity while relatively low hormonal responses suggest receptor hyposensitivity. 328 Many substances with different sites of action have been used in 5-HTergic challenge studies, including L-TRP, 329 fenfluramine, [330][331][332][333][334] buspirone, 335 metachlorophenylpiperazine (m-CPP) 336 and several 5-HTergic reuptake inhibitors. [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.…”

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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“…Buspirone administered orally induces a significant dose-dependent Inerease in PRL levels (Meltzer et al 1983;Anderson and Cowen, 1992;Yatham and Steiner, 1993) Meltzer et al 1992). The administration of buspirone induces a variable ACTH/cortisol release (Neuhauser et al 1988;Yatham and Steiner.…”

Section: Assessment Of 5-htia Reeeptor Funetion In Humans Al D'ipirouementioning

confidence: 99%