Neuroendocrine Effects of a 20-mg Citalopram Infusion in Healthy Males A Placebo-Controlled Evaluation of Citalopram as 5-HT Function Probe

Seifritz, Erich; Baumann, Pierre; Müller, Matthias J.; Annen, Oliver; Amey, M.; Hemmeter, Ulrich; Hatzinger, Martin; Chardon, F.; Holsboer‐Trachsler, Edith

doi:10.1016/0893-133x(95)00117-v

Cited by 97 publications

(83 citation statements)

References 67 publications

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“…This led to the suggestion that LSD acts as a dopamine D 2 receptor agonist in the pituitary. However, the present study in humans found that LSD increased the plasma levels of prolactin and cortisol, which are both markers of serotonergic activity (87,88). Our findings suggest that the serotonergic stimulant effects of LSD on prolactin regulation usurp any dopamine D 2 receptor-mediated inhibition in humans at the dose used in the present study.…”

Section: Autonomic and Endocrine Effectscontrasting

confidence: 43%

Acute Effects of Lysergic Acid Diethylamide in Healthy Subjects

Schmid¹,

Enzler²,

Gasser

et al. 2015

Biological Psychiatry

342

417

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Section: Autonomic and Endocrine Effectscontrasting

confidence: 43%

Acute Effects of Lysergic Acid Diethylamide in Healthy Subjects

Schmid¹,

Enzler²,

Gasser

et al. 2015

Biological Psychiatry

342

417

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“…The results of our study replicate the finding that SSRIs can have an immediate and widespread diminishing impact on interactions of the healthy neural system [Klaassens et al, 2015; Murphy et al, 2009; Schaefer et al, 2014]. In conjunction with other SSRIs, citalopram had clear neuroendocrine effects [Seifritz et al, 1996], but did not induce cognitive or subjective changes as measured with the NeuroCart ® battery. Network effects of galantamine were more discrete and variable over time.…”

Section: Discussionsupporting

confidence: 86%

Time related effects on functional brain connectivity after serotonergic and cholinergic neuromodulation

Klaassens

Rombouts

Winkler

et al. 2016

Human Brain Mapping

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Psychopharmacological research, if properly designed, may offer insight into both timing and area of effect, increasing our understanding of the brain's neurotransmitter systems. For that purpose, the acute influence of the selective serotonin reuptake inhibitor citalopram (30 mg) and the acetylcholinesterase inhibitor galantamine (8 mg) was repeatedly measured in 12 healthy young volunteers with resting state functional magnetic resonance imaging (RS‐fMRI). Eighteen RS‐fMRI scans were acquired per subject during this randomized, double blind, placebo‐controlled, crossover study. Within‐group comparisons of voxelwise functional connectivity with 10 functional networks were examined (P < 0.05, FWE‐corrected) using a non‐parametric multivariate approach with cerebrospinal fluid, white matter, heart rate, and baseline measurements as covariates. Although both compounds did not change cognitive performance on several tests, significant effects were found on connectivity with multiple resting state networks. Serotonergic stimulation primarily reduced connectivity with the sensorimotor network and structures that are related to self‐referential mechanisms, whereas galantamine affected networks and regions that are more involved in learning, memory, and visual perception and processing. These results are consistent with the serotonergic and cholinergic trajectories and their functional relevance. In addition, this study demonstrates the power of using repeated measures after drug administration, which offers the chance to explore both combined and time specific effects. Hum Brain Mapp 38:308–325, 2017. © 2016 Wiley Periodicals, Inc.

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“…[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. 19 Bhagwagar et al 21 showed that the prolactin response to citalopram was blunted similarly in both acutely depressed and recovered drug-free euthymic subjects.…”

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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Neuroendocrine Effects of a 20-mg Citalopram Infusion in Healthy Males A Placebo-Controlled Evaluation of Citalopram as 5-HT Function Probe

Cited by 97 publications

References 67 publications

Acute Effects of Lysergic Acid Diethylamide in Healthy Subjects

Acute Effects of Lysergic Acid Diethylamide in Healthy Subjects

Time related effects on functional brain connectivity after serotonergic and cholinergic neuromodulation

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

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