Article

Mirtazapine Acutely Inhibits Salivary Cortisol Concentrations in Depressed Patients

Department of Psychiatry, University of Munich, Nussbaumstr. 7, 80336 Munich, Germany.
Annals of the New York Academy of Sciences (Impact Factor: 4.31). 01/2005; 1032(1):279-82. DOI: 10.1196/annals.1314.038
Source: PubMed

ABSTRACT Mirtazapine has been shown to acutely inhibit cortisol secretion in healthy subjects. In the current study, the impact of mirtazapine treatment on salivary cortisol secretion was investigated in 12 patients with major depression (DSM-IV criteria). Patients were treated with mirtazapine for 3 weeks, receiving 15 mg of mirtazapine on day 0, 30 mg on day 1, and 45 mg per day from day 2 to the end of the study (day 21). Response to mirtazapine treatment was defined by a reduction of at least 50% in the Hamilton Rating Scale for Depression after 3 weeks of therapy. Salivary cortisol concentrations were measured before treatment (day -1), at the beginning of treatment (day 0), after 1 week (day 7), and after 3 weeks (day 21) of treatment with mirtazapine. Saliva samples were collected hourly from 8 am to 8 pm. A significant reduction in cortisol concentrations was already noted after 1 day of mirtazapine treatment which was comparable in responders and in nonresponders. Mirtazapine therefore appears to be an effective in decreasing hypercortisolism in depression. However, the importance of the acute inhibitory effects of mirtazapine on cortisol secretion for its antidepressant efficacy has to be further clarified.

0 Followers
 · 
105 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Stress is defined as a state that can threaten homeostasis in an organism to initiate the adaptive process. Stress mediators, which include the classic neuroendocrine hormones and a number of neurotransmitters, cytokines, and growth factors, regulate both basal and threatened homeostasis to help control the stress. Severity of stress, as well as malfunctioning of stress pathways, may impair its controllability, leading to the pathogenesis of psychiatric illnesses including depression. Leptin was initially identified as an antiobesity hormone, acting as a negative feedback adiposity signal to control energy homeostasis by binding to its receptors in the hypothalamus. Accumulating evidence has expanded the function of leptin from the control of energy balance to the regulation of other physiological and psychological processes. The aim of this paper is to evaluate the potential role of leptin in stress controllability. To this end, studies on the role of leptin in stress-induced activation of the hypothalamus-pituitary-adrenocortical axis, feeding behavior, learned helplessness, and other depression models have been accumulated. The knowledge accumulated in this article may facilitate the development of alternative treatment strategies, beyond serotonin and noradrenaline reuptake inhibition, for psychiatric care and stress-related disorders.
    Behavioural Pharmacology 07/2014; 25(5-6). DOI:10.1097/FBP.0000000000000050 · 2.19 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Determining the salivary awakening cortisol response (ACR) is a non-invasive, reliable method to detect changes in the hypothalamus-hypopituitary-adrenal (HPA) axis. Although a role of the HPA axis in depression is widely recognized, data on the ACR in depressive patients are still scarce and inconsistent. The present study assessed the ACR in depressed patients admitted for inpatient psychotherapy and a comparison group of other psychiatric diagnoses under the same conditions. The ACR was found to be attenuated in depressed as compared to non-depressed patients. This finding is in contrast to previous studies in healthy subjects or depressed outpatients and suggests a blunted rather than an exacerbated HPA reactivity. Further studies will be needed to disentangle the complex relationship between depression and the ACR.
    Psychoneuroendocrinology 09/2006; 31(7):900-4. DOI:10.1016/j.psyneuen.2006.03.005 · 5.59 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Some depressions are presumed to result from changes in levels of stress-related hormones released from the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system (SNS), represented by adrenocorticotropic hormone (ACTH) and neuropeptide Y (NPY), respectively. Venipuncture for blood sampling has been proposed to be a stress factor that increases circulating ACTH and NPY levels. We examined the effects of mirtazapine on plasma levels of ACTH- and NPY-like immunoreactive substances (IS) in healthy subjects under continual stress induced by repetitive venipunctures for blood sampling. An open-labeled crossover study was conducted on eight healthy volunteers. Each subject was administered a single oral dose of mirtazapine or placebo at an interval of 1 month. Venous blood samples were collected repetitively before and after each administration. Plasma levels of ACTH- and NPY-IS were measured using a highly sensitive enzyme immunoassay. In the placebo group, plasma ACTH-IS levels at 240 min and NPY-IS levels at 40 min increased significantly compared with the levels before administration, presumably due to stress. Oral administration of mirtazapine resulted in significant decreases in plasma ACTH-IS level at 60 and 240 min and NPY-IS level at 20 and 40 min compared with placebo administration. These findings suggest that the antidepressant activity of mirtazapine may involve the suppression of not only the HPA axis but also the SNS.
    01/2012; 2(1):1–5. DOI:10.1016/j.biomag.2011.12.001