24-Hour Profiles of Adrenocorticotropin, Cortisol, and Growth Hormone in Major Depressive Illness: Effect of Antidepressant Treatment*

Linkowski, Paul; Mendlewicz, Julien; Kerkhofs, Myriam; Leclercq, R; Golstein, J.; Brasseur, M; Copinschi, Georges; Cauter, Eve Van

doi:10.1210/jcem-65-1-141

Cited by 293 publications

(118 citation statements)

References 24 publications

Supporting

Mentioning

103

Contrasting

Unclassified

Order By: Relevance

“…The effect of antidepressants on the c-Fos induction in the PVH has been previously reported for different kinds of stressors (Duncan et al, 1996) and is consistent with the clinical effects of antidepressants. Antidepressant administration normalizes HPA hyperactivity that is frequently observed in depressed patients and this effect is related to remission of depressive symptoms (Linkowski et al, 1987). This reduction of the HPA axis is, at least in part, consistent with our results showing a reduction in the c-Fos expression in the PVH and in the LC that send direct excitatory projections to PVH (Duman et al, 1994).…”

Section: Imipraminesupporting

confidence: 91%

Stress-Induced c-Fos Expression is Differentially Modulated by Dexamethasone, Diazepam and Imipramine

Medeiros

Reis

Mello

2005

Neuropsychopharmacol

View full text Add to dashboard Cite

Immobilization stress upregulates c-Fos expression in several CNS areas. Repeated stress or the use of drugs can modulate stressinduced c-Fos expression. Here, we investigated in 40 different areas of the rat brain the effects of dexamethasone (SDX, a synthetic glucocorticoid), diazepam (SBDZ, a benzodiazepine), and imipramine (IMI, an antidepressant) on the c-Fos expression induced by restraint stress. Wistar rats were divided into four groups and submitted to 20 days of daily injection of saline (three first groups) or imipramine, 15 mg/kg, i.p. On day 21, animals were submitted to injections of saline (somatosensory, SS), SDX (1 mg/kg, i.p.), SBDZ (5 mg/kg, i.p.), or IMI (15 mg/kg, i.p.) before being submitted to restraint. Immediately after stress, the animals were perfused and their brains processed with immunohistochemistry for c-Fos (Ab-5 Oncogene Science). Dexamethasone reduced stress-induced c-Fos expression in SS cortex, hippocampus, paraventricular nucleus of the hypothalamus (PVH), and locus coeruleus (LC), whereas diazepam reduced c-Fos staining in the SS cortex, hippocampus, bed nucleus of stria terminalis, septal area, and hypothalamus (preoptic area and supramammillary nucleus). Chronic administration of imipramine decreased staining in the hippocampus, PVH, and LC, while increasing it in the nucleus raphe pallidus. We conclude that dexamethasone, diazepam and imipramine differentially modulate stress-induced Fos expression. The present study provides an important comparative background that may help in the further understanding of the effects of these compounds and on the brain activation as well as on the behavioral, neuroendocrine, and autonomic responses to stress.

show abstract

Section: Imipraminesupporting

confidence: 91%

Stress-Induced c-Fos Expression is Differentially Modulated by Dexamethasone, Diazepam and Imipramine

Medeiros

Reis

Mello

2005

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…This is in contrast to the finding that ACTH was blunted after mirtazapine in normal controls (Laakmann et al, 1999;Schüle et al, 2002b). Elevated nocturnal cortisol (Linkowski et al, 1987;Steiger et al, 1989) and ACTH (Linkowski et al, 1987) levels are robust findings in acutely depressed patients and mirror HPA overactivity in affective disorders. Cortisol levels decreased after recovery in drug-free patients (Steiger et al, 1989) and after a 4-week treatment of depressed patients with trimipramine but not with imipramine (Sonntag et al, 1996).…”

Section: Discussioncontrasting

confidence: 74%

Changes of Sleep Architecture, Spectral Composition of Sleep EEG, the Nocturnal Secretion of Cortisol, ACTH, GH, Prolactin, Melatonin, Ghrelin, and Leptin, and the DEX-CRH Test in Depressed Patients during Treatment with Mirtazapine

Schmid

Wichniak

Uhr

et al. 2005

Neuropsychopharmacol

143

View full text Add to dashboard Cite

The noradrenergic and specific serotoninergic antidepressant mirtazapine improves sleep, modulates hormone secretion including blunting of hypothalamic-pituitary-adrenocortical (HPA) activity, and may prompt increased appetite and weight gain. The simultaneous investigation of sleep electroencephalogram (EEG) and hormone secretion during antidepressive treatment helps to further elucidate these effects. We examined sleep EEG (for later conventional and quantitative analyses) and the nocturnal concentrations of cortisol, adrenocorticotropin (ACTH), growth hormone (GH), prolactin, melatonin and the key factors of energy balance, ghrelin, and leptin before and after 28 days of treatment of depressed patients (seven women, three men, mean age 39.974.2 years) with mirtazapine. In addition, a sleep EEG was recorded at day 2 and the dexamethasone-corticotropin-releasing hormone (DEX-CRH) test was performed to assess HPA activity at days À3 and 26. Psychometry and mirtazapine plasma concentrations were measured weekly. Already at day 2, sleep continuity was improved. This effect persisted at day 28, when slow-wave sleep, low-delta, theta and alpha activity, leptin and (0300-0700) melatonin increased, and cortisol and ghrelin decreased. ACTH and prolactin remained unchanged. The first two specimens of GH collected after the start of quantitative EEG analysis were reduced at day 28. The DEX-CRH test showed, at day 26, a blunting of the overshoot of ACTH and cortisol found at day À3. The Hamilton Depression score decreased from 32.177.3 to 15.576.7 between days À1 and 28. A weight gain of approximately 3 kg was observed. This unique profile of changes is compatible with the action of mirtazapine at 5-HT-2 receptors, at presynaptic adrenergic alpha 2 receptors, at the HPA system, and on ghrelin and leptin.

show abstract

“…increased duration of the first REM period and increased REM This seems to fit with the increased intensity of nonREM-todensity (Reynolds and Kupfer 1987;Linkowski et al 1987; REM transitions when cortisol levels are high (see Fig. 4d).…”

Section: +Other Terms) (5) Sample and Data Generationmentioning

confidence: 60%

Modelling and exploring human sleep with event history analysis

Yassouridis

Steiger

Klinger³

et al. 1999

Journal of Sleep Research

View full text Add to dashboard Cite

SUMMARYIn this paper we propose the use of statistical models of event history analysis for investigating human sleep. These models provide appropriate tools for statistical evaluation when sleep data are recorded continuously over time or on a fine time grid, and are classified into sleep stages such as REM and nonREM as defined by Rechtschaffen and Kales (1968). In contrast to conventional statistical procedures, event history analysis makes full use of the information contained in sleep data , and can therefore provide new insights into non-stationary properties of sleep. Probabilities of or intensities for transitions between sleep stages are the basic quantities for characterising sleep processes. The statistical methods of event history analysis aim at modelling and estimating these intensities as functions of time, taking into account individual sleep history and assessing the influence of factors of interest, such as hormonal secretion. In this study we suggest the use of non-parametric approaches to reveal unknown functional forms of transition intensities and to explore timevarying and non-stationary effects. We then apply these techniques in a study of 30 healthy male volunteers to assess the mean population intensity and the effects of plasma cortisol concentration on the transition between selected sleep stages as well as the influence of elapsed time in a current REM period on the intensity for a transition to nonREM. The most interesting findings are that (a) the intensity of the nonREM-to-REM transitions after sleep onset in young men shows a periodicity which is similar to that of nonREM/REM cycles; (b) 30-45 min after sleep onset, young men reveal a great propensity to pass from light sleep (stages 1 or 2) into slowwave sleep (SWS) (stages 3 or 4); (c) high cortisol levels imposed additional impulses on the transition intensity of (i) wake to sleep around 2 h after sleep onset, (ii) nonREM to REM around 6 h later, (iii) stage 1 or stage 2 sleep to SWS around 2, 4 and 6 h later and (iv) SWS to stage 1 or stage 2 sleep about 2 h later. Moreover, high cortisol concentrations at the beginning of REM periods favoured the change to nonREM sleep, whereas later their influence on a nonREM change became weak and weaker. As sleep data are also available as event-oriented data in many studies in sleep research, event history analysis applied additionally to conventional statistical procedures, such as regression analysis or analyis of variance, could help to acquire more information and knowledge about the mechanisms behind the sleep process. event history analysis, relative intensity, sleep, cortisol

show abstract

24-Hour Profiles of Adrenocorticotropin, Cortisol, and Growth Hormone in Major Depressive Illness: Effect of Antidepressant Treatment*

Cited by 293 publications

References 24 publications

Stress-Induced c-Fos Expression is Differentially Modulated by Dexamethasone, Diazepam and Imipramine

Stress-Induced c-Fos Expression is Differentially Modulated by Dexamethasone, Diazepam and Imipramine

Changes of Sleep Architecture, Spectral Composition of Sleep EEG, the Nocturnal Secretion of Cortisol, ACTH, GH, Prolactin, Melatonin, Ghrelin, and Leptin, and the DEX-CRH Test in Depressed Patients during Treatment with Mirtazapine

Modelling and exploring human sleep with event history analysis

Contact Info

Product

Resources

About