Review of the results from clinical studies on the efficacy, safety and tolerability of mirtazapine for the treatment of patients with major depression

Fawcett, Jan; Barkin, Robert L.

doi:10.1016/s0165-0327(98)00224-9

Cited by 202 publications

(176 citation statements)

References 60 publications

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“…Similar effects were observed after selective stimulation of 5-HT1 receptors with ipsapirone (Seifritz et al, 1996). The enhancement of serotoninergic neurotransmission resulting from 5-HT2 blockade by mirtazapine is specifically mediated via 5-HT1 receptors (Fawcett and Barkin, 1998). This explains the similarities between ipsapirone and mirtazapine in their influence on the sleep-EEG spectrum.…”

Section: Discussionsupporting

confidence: 54%

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

146

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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.

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Section: Discussionsupporting

confidence: 54%

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

146

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“…These 'atypical' drugs (mirtazapine, mianserin, nefazodone, and trazodone) have been shown to have antidepressant efficacy in multiple double-blind, placebocontrolled studies (Pinder and Fink, 1982;Marek et al, 1992;Davis et al, 1997;Fawcett and Barkin, 1998). The common potent pharmacological target for these agents is blockade of the 5-HT 2 family of receptors.…”

Section: Other 5-ht 2 Antagonists: Spectrum Of Clinical Activitymentioning

confidence: 99%

Synergistic Action of 5-HT2A Antagonists and Selective Serotonin Reuptake Inhibitors in Neuropsychiatric Disorders

Marek

Carpenter

McDougle

et al. 2002

Neuropsychopharmacol

241

120

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Recently, the addition of drugs with prominent 5-HT 2 receptor antagonist properties (risperidone, olanzapine, mirtazapine, and mianserin) to selective serotonin reuptake inhibitors (SSRIs) has been shown to enhance therapeutic responses in patients with major depression and treatment-refractory obsessive-compulsive disorder (OCD). These 5-HT 2 antagonists may also be effective in ameliorating some symptoms associated with autism and other pervasive developmental disorders (PDDs). At the doses used, these drugs would be expected to saturate 5-HT 2A receptors. These findings suggest that the simultaneous blockade of 5-HT 2A

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“…In this regard, detailed mutational analysis of different GPCRs has demonstrated the role of this intracellular loop 3 playing a key role in determining receptor-G protein coupling in conjunction with residues present in the intracellular loop 2 [25,137,184]. In the therapeutic context, the 2 -adrenoceptor antagonist mirtazapine is prescribed for the treatment of patients with major depression with positive results [53,54].…”

Section: G Protein-coupled Receptors In Depressed Suicide Brain: Funcmentioning

confidence: 99%

Heterotrimeric G Proteins: Insights into the Neurobiology of Mood Disorders

González-Maeso

Meana²

2006

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Mood disorders such as major depression and bipolar disorder are common, severe, chronic and often lifethreatening illnesses. Suicide is estimated to be the cause of death in up to approximately 10-15% of individuals with mood disorders. Alterations in the signal transduction through G protein-coupled receptor (GPCR) pathways have been reported in the etiopathology of mood disorders and the suicidal behavior. In this regard, the implication of certain GPCR subtypes such as 2A -adrenoceptor has been repeatedly described using different approaches. However, several discrepancies have been recently reported in density and functional status of the heterotrimeric G proteins both in major depression and bipolar disorder. A compilation of the most relevant research topics about the implication of heterotrimeric G proteins in the etiology of mood disorders (i.e., animal models of mood disorders, studies in peripheral tissue of depressive patients, and studies in postmortem human brain of suicide victims with mood disorders) will provide a broad perspective of this potential therapeutic target field. Proposed causes of the discrepancies reported at the level of G proteins in postmortem human brain of suicide victims will be discussed.

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Review of the results from clinical studies on the efficacy, safety and tolerability of mirtazapine for the treatment of patients with major depression

Cited by 202 publications

References 60 publications

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

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

Synergistic Action of 5-HT2A Antagonists and Selective Serotonin Reuptake Inhibitors in Neuropsychiatric Disorders

Heterotrimeric G Proteins: Insights into the Neurobiology of Mood Disorders

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