H.-W. Clement

Bio: H.-W. Clement is an academic researcher from University of Marburg. The author has contributed to research in topics: Raphe nuclei & Dopaminergic. The author has an hindex of 13, co-authored 21 publications receiving 581 citations.

White blood cells and cortisol after sleep deprivation and recovery sleep in humans.

Abstract: Sleep deprivation (SD) has enriched our treatment programme for major depression. SD has been demonstrated to modify different host defence activities. There is some evidence that there are reciprocal relationships between immune function and increased hypothalamic-pituitary-adrenocortical (HPA) axis activity in depression. We therefore investigated the number of leukocytes, granulocytes, monocytes, lymphocytes, B cells, T cells, helper T cells, cytotoxic T cells, NK cells and salivary cortisol in 10 healthy men before and after total SD (TSD) as well as after recovery sleep. Blood samples were drawn on 3 consecutive days at 7 am, 1 pm and 7 pm, respectively. Comparison of the 7 am values by contrast analysis yielded significant differences for granulocytes (p = 0.044) and NK cells (p = 0.001) after SD and recovery sleep. NK cells decreased and granulocytes increased after SD and after recovery sleep. Significant differences between single points in time across the day were found for granulocytes (p = 0.022), monocytes (p = 0.031), T cells (p = 0.005), helper T cells (p = 0.004), cytotoxic T cells (p = 0.005) and NK cells (p = 0.017). No significant difference could be detected for leukocytes, lymphocytes and B cells counts. These results favour the thesis that SD and recovery sleep lead to changes in the distribution of peripheral leukocytes, especially in a reduction of NK cells after SD and recovery sleep. The cortisol rhythm was affected neither by SD nor recovery sleep.

Serotonin-norepinephrine interactions: a voltammetric study on the effect of serotonin receptor stimulation followed in the N. raphe dorsalis and the Locus coeruleus of the rat.

Abstract: In vivo voltammetry with carbon fibre electrodes was used to study the effect of the serotoninergic (5-HT) neuronal system on the noradrenergic (NE) system in the Locus coeruleus of the rat. The voltammetric DOPAC signal in the Locus coeruleus, used as a measure of NE neuronal activity, was increased after systemic application of the 5-HT1B agonist CGS-12066B, the 5-HT2 antagonist ritanserin, and, to a lesser extent, by ipsapirone, a 5-HT1A agonist. The findings suggest that the NE neuronal system of the Locus coeruleus is stimulated by 5-HT1A and 5-HT1B receptor activation and inhibited by 5-HT2 receptors. Likewise the 5-HT releaser and uptake inhibitor fenfluramine increased the DOPAC level in the Locus coeruleus. In contrast to the 5-HT1 agonists, which reduced 5-hydroxyindoleacetic acid (5-HIAA) in the Nucleus raphe dorsalis, ritanserin increased the 5-HIAA signal in this nucleus. This finding could help to explain the action of ritanserin as sleep-modulating substance.

Effects of interferon-gamma, interleukin-1 beta, and tumor necrosis factor-alpha on the serotonin metabolism in the nucleus raphe dorsalis of the rat.

Abstract: The effects of the cytokines interferon (IFN)-γ, interleukin (IL)-1, and tumor necrosis factor (TNF)-α on the serotoninergic transmission in the nucleus raphe dorsalis (NRD) were studied after peripheral and central application. The studies were performed in the freely moving rat using differential pulse voltammetry with multicarbon fibre electrodes to study the extracellular levels of the serotonin (5-HT) metabolite 5-hydroxyindoleacetic acid (5-HIAA). The extracellular 5-HIAA levels were not changed in the NRD after peripheral application of rat recombinant IFN-γ, but elevated by the cytokines IL-1β and TNF-α. After intracerebroventricular (i.c.v.) application the cytokines IFN-γ, IL-1β and TNF-α stimulated the serotoninergic transmission in the NRD. Our data suggest that the effect of peripherally elevated cytokine concentrations on the serotonin metabolism in the NRD of the rat is cytokine-dependent. In this respect the T-cell and NK-cell cytokine IFN-γ acts clearly different when compared to the mainly macrophage-derived cytokines IL-1β and TNF-α, and plays a different role in the communication between immune and central nervous system.

Major depression and activation of the inflammatory response system.

Abstract: Contemporary models of major depression emphasize the role of hypothalamic-pituitary-adrenal (HPA)-axis hyperactivity and of dysfunctions in the turnover of serotonin (5-HT) or catecholamines in the etiopathogenesis of major depression. Contemporary models of major depression do not incorporate the effects of the inflammatory response system (IRS), even though the IRS powerfully influences HPA-axis activity, 5-HT and catecholaminergic turnover and even though activation of the IRS may induce depression-like behavior in animals and humans. There is now evidence that major depression is accompanied by a moderate activation of the IRS (reviews: Maes, 1993; 1995; 1997; Maes, Smith, & Scharpe, 1995c; Holden, Pakula, & Mooney, 1997; Maes & Smith, 1997; Connor & Leonard, 1998; Maier & Watkins, 1998). In this paper we propose a concise IRS model of major depression.

Autoregulation of Serotonin Neurons: Role in Antidepressant Drug Action

Abstract: The existence of an endogenous vasoconstrictor in blood serum ([Stevens and Lee, 1984][1]; [Brodie, 1900][2]) and the presence in the gut of a substance that increases intestinal motility ([Vialli and Ersparmer, 1933][3]) had been known to scientists since the beginning of the century. However, it