The citalopram challenge test in patients with major depression and in healthy controls

Kapitany, T.; Schindl, Monika; Schindler, S.D.; Heßelmann, B.; Füreder, T.; Barnas, C.; Sieghart, Werner; Kasper, Siegfried

doi:10.1016/s0165-1781(99)00082-7

Cited by 68 publications

(64 citation statements)

References 46 publications

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“…The study was not randomized because if the citalopram were administered first, there might be carryover effects of the drug to the second scan. As pointed out by Kapitany et al (1999), a time interval of at least 3 weeks would be necessary between placebo and citalopram conditions due to the known carryover effects of serotonergic drugs. As this paradigm was intended for application to studies of psychiatric patients and it would not be possible to maintain patients unmedicated during such a long time interval, the citalopram was administered on the first day of study.…”

Section: Methodsmentioning

confidence: 99%

Effects of Serotonin Transporter Promoter Polymorphisms on Serotonin Function

Smith

Lotrich

Malhotra

et al. 2004

Neuropsychopharmacol

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The serotonin transporter promoter polymorphism (5-HTTLPR) has been associated with vulnerability to stress-induced depressive symptoms and with the speed and rate of response to antidepressant treatment. The goal of the present study was to evaluate the association between the 5-HTTLPR and the functional response of the serotonin system as measured by the neuroendocrine and cerebral metabolic response to intravenous administration of the selective serotonin reuptake inhibitor citalopram in normal control subjects. Genotyping was performed for 5-HTTLPR insertion/deletion polymorphism long (l) and short (s) variant alleles. The ll genotype was compared with the combined sl þ ss and with the ss genotype alone. Citalopram plasma concentrations did not differ significantly between groups. The s allele was associated with a less of an increase in prolactin and cortisol than the ll genotype. The s allele was associated with greater decreases in left frontal, precentral and middle temporal gyri compared to the ll genotype. The ll genotype was associated with greater decreases in right frontal, insula and superior temporal gyrus compared to the ss genotype. These findings suggest that 5-HTTLPR is associated with an altered functional response of the serotonin system, which may represent a neurobiologic substrate for the differential response to antidepressant treatment in late life and the emergence of neuropsychiatric symptoms in neurodegenerative disorders.

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Section: Methodsmentioning

confidence: 99%

Effects of Serotonin Transporter Promoter Polymorphisms on Serotonin Function

Smith

Lotrich

Malhotra

et al. 2004

Neuropsychopharmacol

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“…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. The cortisol responses, however, were blunted in the acutely depressed patients, but not in the recovered subjects.…”

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

confidence: 98%

“…[15][16][17][18] Furthermore, depressed and remitted patients show blunted neuroendocrine responses to drugs that stimulate 5-HT turnover, suggesting decreased 5-HT responsiveness. [19][20][21] Some 5-HT abnormalities are also seen in remitted depressed patients or in subjects with a family history of depression, suggesting that either some dysfunction in 5-HT systems or an increased sensitivity of the 5-HT system is a trait abnormality in depression. It should be mentioned, however, that not all depressed patients show all these abnormalities in 5-HTergic functioning.…”

Section: Involvement Of Serotonin In Depressionmentioning

confidence: 99%

“…These tests involve the administration of a 5-HTergic probe and the subsequent assessment of one or more anterior pituitary hormones, such as cortisol, ACTH, growth hormone and prolactin. 19,20 The secretion of prolactin is regulated by 5-HTergic mechanisms in the brain. 322,323 Therefore, increased plasma prolactin can be interpreted as an index of enhanced brain serotonin function 324,325 and hypersensitivity of the 5-HTergic system.…”

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

confidence: 99%

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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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“…Depression is schematically associated with a general increase in cholinergic and decrease in serotonergic neurotransmission (Gillin et al, 1991;Hasler et al, 2004;Kapitany et al, 1999;Seifritz et al, 1998). To test for the presence of such imbalance between cholinergic and serotonergic function in H mice, we investigated the sleep modifications induced by treatments with agonists of muscarinic and serotonergic 5-HT 1A receptors in both H and NH mice.…”

Section: Introductionmentioning

confidence: 99%

Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

Popa

Yacoubi²,

Vaugeois³

et al. 2005

Neuropsychopharmacol

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In depressed patients, sleep undergoes marked alterations, especially sleep onset insomnia, sleep fragmentation, and disturbances of the Rapid Eye Movement (REM) sleep. Abnormalities of rest-activity rhythms and of hypothalamic-pituitary-adrenocortical function have also been described in these patients. In the present study, we examined the presence of such abnormalities in a recently developed line of mice (Helpless mice-H) that exhibit depression-like behaviors in validated tests, compared to the nonhelpless (NH) line derived from the same colony. Experiments were essentially carried out in females for which previous studies showed marked differences between H and NH lines. Compared to NH mice, the H line exhibited (i) lower basal locomotor activity, (ii) sleep fragmentation, shift towards lighter sleep stages, and facilitation of REM sleep reflected by increased amounts and decreased latency, (iii) larger response to the REM sleep promoting effect of muscarinic receptor stimulation (by arecoline). In contrast, H and NH mice were equally responsive to the REM sleep inhibitory effect of 5-HT 1A receptor stimulation (by 8-OH-DPAT). In addition, a deficiency in delta power enhancement after sleep deprivation was observed in the H group, and acute immobilization stress in this group failed to elicit a REM sleep rebound and was associated with a long-lasting raise in serum corticosterone levels. These results further validate H mice as a depression model and suggest they might be of particular interest for investigating the neurobiological mechanisms and possibly genetic substrates underlying sleep alterations associated with depression.

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The citalopram challenge test in patients with major depression and in healthy controls

Cited by 68 publications

References 46 publications

Effects of Serotonin Transporter Promoter Polymorphisms on Serotonin Function

Effects of Serotonin Transporter Promoter Polymorphisms on Serotonin Function

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

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