Melatonin, cortisol and ACTH in patients with major depressive disorder and healthy humans with special reference to the outcome of the dexamethasone suppression test

Beck-Friis, Johan; Ljunggren, Jan‐Gustaf; Thorén, Marja; Rosen, Dietrich von; Kjellman, Bengt; Wetterberg, Lennart

doi:10.1016/0306-4530(85)90055-1

Cited by 126 publications

(55 citation statements)

References 22 publications

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“…Antidepressant-like effects of melatonin have also been reported in the forced swim test (Overstreet et al, 1998;Shaji and Kulkarni, 1998;Raghavendra et al, 2000). The clinical studies with melatonin and depression are less clear as, for example, both decreases (Beck-Friis et al, 1985;Brown et al, 1985;Zetin et al, 1987) as well as increases (Claustrat et al, 1984;Thompson et al, 1988;Sekula et al, 1997) in melatonin secretion have been reported in patients with diagnosis of major depression. Moreover, although a relation between melatonin levels and depression has been reported by Souetre et al (1989), this has not been confirmed by other authors (Beck-Friis et al, 1995;Rubin et al, 1992;Szymanska et al, 2001).…”

Section: Discussionmentioning

confidence: 98%

Effect of Agomelatine in the Chronic Mild Stress Model of Depression in the Rat

Papp

Gruca

Boyer

et al. 2002

Neuropsychopharmacol

242

166

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Chronic mild stress (CMS), a well-validated model of depression, was used to study the effects of the melatonin agonist and selective 5-HT 2C antagonist agomelatine (S 20098) in comparison with melatonin, imipramine, and fluoxetine. All drugs were administered either 2 h before (evening treatment) or 2 h after (morning treatment) the dark phase of the 12-h light/dark cycle. Chronic (5 weeks) evening treatment with agomelatine or melatonin (both at 10 and 50 mg/kg i.p.) dose-dependently reversed the CMS-induced reduction in sucrose consumption. The magnitude and time course of the action of both drugs was comparable to that of imipramine and fluoxetine (both at 10 mg/kg i.p.); however, melatonin was less active than agomelatine at this dose. The effect of evening administration of agomelatine and melatonin was completely inhibited by an acute injection of the MT 1 /MT 2 antagonist, S 22153 (20 mg/kg i.p.), while the antagonist had no effect in animals receiving fluoxetine or imipramine. When the drugs were administered in the morning, agomelatine caused effects similar to those observed after evening treatment (with onset of action faster than imipramine) but melatonin was ineffective. Moreover, melatonin antagonist, S 22153, did not modify the intakes in stressed animals receiving morning administration of agomelatine and in any other control and stressed groups tested in this study. These data demonstrate antidepressant-like activity of agomelatine in the rat CMS model of depression, which was independent of the time of drug administration. The efficacy of agomelatine is comparable to that of imipramine and fluoxetine, but greater than that of melatonin, which had no antidepressant-like activity after morning administration. While the evening efficacy of agomelatine can be related to its melatonin receptors agonistic properties, its morning activity, which was not inhibited by a melatonin antagonist, indicates that these receptors are certainly required, but not sufficient to sustain the agomelatine efficacy. It is therefore suggested that the antidepressant-like activity of agomelatine depends on some combination of its melatonin agonist and 5-HT 2C antagonist properties.

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Section: Discussionmentioning

confidence: 98%

Effect of Agomelatine in the Chronic Mild Stress Model of Depression in the Rat

Papp

Gruca

Boyer

et al. 2002

Neuropsychopharmacol

242

166

View full text Add to dashboard Cite

show abstract

“…As circadian alterations have been described in monoaminergic secretion (Morin, 1999;Wirz-Justice, 1987), in hypothalamic-pituitary-adrenal axis hormones (Beck-Friis et al, 1985;Linkowski et al, 1987), and in immune system components such as cytokines (Humphreys et al, 2006), the chronobiological disturbances may act as an essential link in the pathogenesis of MD, complementing other etiopathogenical pathways and integrating its multidirectional interactions.…”

Section: Discussionmentioning

confidence: 99%

Differential Association of Circadian Genes with Mood Disorders: CRY1 and NPAS2 are Associated with Unipolar Major Depression and CLOCK and VIP with Bipolar Disorder

Soria

Martínez‐Amorós

Escaramís

et al. 2010

Neuropsychopharmacol

312

203

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Disruptions in circadian rhythms have been described in mood disorders (MD), but the involvement of genetic variation in genes pertaining to the molecular circadian machinery in the susceptibility to MD has not been conclusively determined. We examined 209 single-nucleotide polymorphisms (SNPs) covering 19 circadian genes (ADCYAP1, ARNTL, ARNTL2, BHLHB2, BHLHB3, CLOCK, CRY1, CRY2, CSNK1E, DBP, NPAS2, NR1D1, PER1, PER2, PER3, RORA, TIMELESS, VIP, and VIPR2) in a sample of 534 MD patients (335 with unipolar major mood depression (MDD) and 199 with bipolar disorder (BD)) and 440 community-based screened controls. Nominally, statistically significant associations were found in 15 circadian genes. The gene-wide test, corrected for the number of SNPs analyzed in each gene, identified significant associations in CRY1 (rs2287161), NPAS2 (rs11123857), and VIPR2 (rs885861) genes with the combined MD sample. In the MDD subsample, the same SNPs in CRY1 and NPAS2 of the combined sample remained associated, whereas in the BD subsample CLOCK (rs10462028) and VIP (rs17083008) were specifically associated. The association with an SNP located 3 0 near CRY1 gene in MDD remained statistically significant after permutation correction at experiment level (p ¼ 0.007). Significant additive effects were found between the SNPs that were statistically significant at the gene-wide level. We also found evidence of associations between two-marker haplotypes in CRY1 and NPAS2 genes and MD. Our data support the contribution of the circadian system to the genetic susceptibility to MD and suggest that different circadian genes may have specific effects on MD polarity.

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“…[3][4][5][6][7][8] Depressed patients often exhibit resting hypercortisolemia, and failure of appropriate negative feedback as measured by the dexamethasone suppression test. [9][10][11][12][13][14][15] There is considerable phenotypic overlap between unipolar depression, bipolar depression and some aspects of schizophrenia (flat affect, anhedonia and other negative symptoms). Subjects with bipolar disorder and schizophrenia also may have hypercortisolemia.…”

Section: Introductionmentioning

confidence: 99%

Regional specificity of brain glucocorticoid receptor mRNA alterations in subjects with schizophrenia and mood disorders

et al. 2002

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Glucocorticoid receptors (GR) mediate the direct effects of glucocorticoids released in response to stress and the regulation of the hypothalamic-pituitary-adrenocortical (HPA) system through a negative feedback mechanism. Individuals with major mental illness, who often exhibit hypercortisolemia, may have down-regulated levels of GR mRNA. In situ hybridization for GR mRNA was performed on post-mortem specimens from patients suffering from depression, bipolar disorder, schizophrenia and from normal controls (n = 15 per group). In frontal cortex, GR mRNA levels were decreased in layers III-VI in the subjects with depression and schizophrenia. In inferior temporal cortex, GR mRNA levels were decreased in layer IV in all three diagnostic groups. In the entorhinal cortex, GR mRNA levels were decreased in layers III and VI in the bipolar group. In hippocampus, GR mRNA levels were reduced in the dentate gyrus, CA 4 , CA 3 and CA 1 in the schizophrenia group. In the subiculum, GR mRNA levels were reduced in the bipolar group. These results suggest that GR dysregulation occurs in all three major psychiatric illnesses with variability according to anatomical site. The severity and heterogeneity of this reduction may underlie some of the clinical heterogeneity seen in these disorders. Molecular Psychiatry (2002) 7, 985-994.

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Melatonin, cortisol and ACTH in patients with major depressive disorder and healthy humans with special reference to the outcome of the dexamethasone suppression test

Cited by 126 publications

References 22 publications

Effect of Agomelatine in the Chronic Mild Stress Model of Depression in the Rat

Effect of Agomelatine in the Chronic Mild Stress Model of Depression in the Rat

Differential Association of Circadian Genes with Mood Disorders: CRY1 and NPAS2 are Associated with Unipolar Major Depression and CLOCK and VIP with Bipolar Disorder

Regional specificity of brain glucocorticoid receptor mRNA alterations in subjects with schizophrenia and mood disorders

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