Noradrenergic function and hypothalamic-pituitary-adrenal axis activity in primary unipolar major depressive disorder

Villiers, A. S. De; Russell, Vivienne A.; Carstens, Machteld E.; Aalbers, Cor; Gagiano, C. A.; Chalton, D. O.; Taljaard, J. J. F.

doi:10.1016/0165-1781(87)90100-4

Cited by 37 publications

(18 citation statements)

References 58 publications

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“…Like de Villiers et al (1987) and Roy et al (1988) we found that HPA-axis variables and sympathoadrenal system activity are intertwined during depression. The lack of a positive correlation between MHPG excretion and HPAaxis activity is in line with the findings of some (Davis et al, 1981;Sternbach et al, 1983;Warsh et al, 1985;Loo et al, 1988;Mazure et al, 1987;Maes et al, 1987a) but not all researchers (Stokes et al, 1981;Rosenbaum et al, 1983).…”

Section: Catecholamine System and Hpa-axis Interrelationshipsmentioning

confidence: 85%

“…In accordance with other authors (Roy et a1.,1985(Roy et a1., , 1988Koslow et al, 1983;Maas et al, 1987;de Villiers et al, 1987) we found a higher sympathoadrenal system (noradrenaline, adrenaline) activity in severely depressed patients. It has been suggested that these findings may be caused by an increased catecholaminergic synthesis by, and release from adrenergic tissues .…”

Section: Dsm-iii Classificationmentioning

confidence: 88%

“…For example, significant positive correlations between indices of sympathetic outflow (plasma of urinary catecholamines or MHPG) and HPA-axis measurements (basal plasma cortisol, UFC, postdexamethasone cortisol) were observed in depressive patients (Stokes et al, 1981;Jimerson et al, 1983;Rosenbaum et al, 1983;Rubin et al, 1985;Roy et al, 1986Roy et al, , 1988de Villiers et al, 1987;Zhou et al, 1987;Garvey et al, 1988;Maes et al, 1990d). Accordingly, it has been proven that depressed patients who failed to suppress cortisol normally in response to 1 mg dexamethasone exhibit a higher sympathoadrenal system activity as compared with cortisol suppressors (Roy et al, 1988;Maes et al, 1990d).…”

Section: Introductionmentioning

confidence: 94%

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Coexisting dysregulations of both the sympathoadrenal system and hypothalamic-pituitary-adrenal-axis in melancholia

Maes¹,

Minner²,

Suy³

et al. 1991

J. Neural Transmission

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In order to delineate putatively coexisting dysregulations between sympathoadrenal system and hypothalamic-pituitary-adrenal (HPA)-axis during depression, the authors measured the following: the pre and postdexamethasone (1 mg) 24 hr urine excretion of noradrenaline, dopamine, adrenaline, 3-methoxy-4-hydroxyphenylglycol (MHPG), free cortisol (UFC), and plasma cortisol. Melancholic patients were characterized by a significantly higher excretion of noradrenaline, dopamine and adrenaline, combined with significantly increased UFC, postdexamethasone plasma cortisol, and UFC values. We found significant and positive correlations between UFC on the one hand, and the 24hr urine excretion of noradrenaline, dopamine, and adrenaline, on the other. By the same token, we established significant relationships between the 24 hr urine excretion of those catecholamines and the postdexamethasone UFC and plasma cortisol values. Cortisol nonsuppressors exhibited a significantly higher excretion of noradrenaline, dopamine and adrenaline, as compared with cortisol suppressors. Dexamethasone administration did not have a significant effect on the urinary output of noradrenaline, dopamine, adrenaline or MHPG.

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Section: Catecholamine System and Hpa-axis Interrelationshipsmentioning

confidence: 85%

Section: Dsm-iii Classificationmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 94%

See 1 more Smart Citation

Coexisting dysregulations of both the sympathoadrenal system and hypothalamic-pituitary-adrenal-axis in melancholia

Maes¹,

Minner²,

Suy³

et al. 1991

J. Neural Transmission

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show abstract

“…Noradrenergic mechanisms were the first to be studied intensively in MDD (Schildkraut, 1965). Early studies reported elevations in the plasma (Barnes et al, 1983;de Villiers et al, 1987;Louis et al, 1975;Roy et al, 1988Roy et al, , 1985Rudorfer et al, 1985;Wyatt et al, 1971), urine (Maas et al, 1987), and cerebrospinal fluid (CSF) (Wong et al, 2000) noradrenaline levels. Noradrenaline kinetic analyses revealed an increased rate of noradrenaline appearance in the extravascular and vascular compartments in MDD patients, but similar rates of noradrenaline clearance in depressed patients and controls (Veith et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Effects of a α2C-Adrenoreceptor Gene Polymorphism on Neural Responses to Facial Expressions in Depression

Neumeister

Drevets

Belfer

et al. 2006

Neuropsychopharmacol

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Alterations in processing of emotionally salient information have been reported in individuals with major depressive disorder (MDD). Evidence suggests a role for noradrenaline in the regulation of a cortico-limbic-striatal circuit that has also been implicated in the pathophysiology of MDD. Herein, we studied the physiological consequences of a common coding polymorphism of the gene for the a 2C -adrenoreceptor (AR) subtypeFthe deletion of four consecutive amino acids at codons 322-325 of the a2C-AR (a2CDel322-325-AR) in medication-free, remitted individuals with MDD (rMDD), and healthy control subjects. After injection of 10 mCi of H 2 15 O, positron emission tomography (PET) measures of neural activity were acquired while subjects were viewing unmasked sad, happy, and fearful faces. The neural responses to sad facial expressions were increased in the amygdala and decreased in the left ventral striatum in rMDD patients relative to healthy control subjects. Furthermore, we report that rMDD carriers of one or two copies of the a2CDel322-325-AR exhibit greater amygdala as well as pregenual and subgenual anterior cingulate gyrus neuronal activity in response to sad faces than healthy a2CDel322-325-AR carriers and rMDD noncarriers. These results suggest that the a2CDel322-325-AR confers a change in brain function implicating this a2-AR subtype into the pathophysiology of MDD.

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“…Pacientes com depressão apresentam níveis de NE plasmática maiores comparados a controles, o que indica hiperatividade simpática na depressão (Wyatt et al, 1971;Lake et al, 1982;Roy et al, 1985;DeVilliers et al, 1987;Gold et al 2005). …”

Section: Disfunção De Sistema Nervoso Autonômicounclassified

Avaliação de sistema nervoso simpático em pacientes deprimidos

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Noradrenergic function and hypothalamic-pituitary-adrenal axis activity in primary unipolar major depressive disorder

Cited by 37 publications

References 58 publications

Coexisting dysregulations of both the sympathoadrenal system and hypothalamic-pituitary-adrenal-axis in melancholia

Coexisting dysregulations of both the sympathoadrenal system and hypothalamic-pituitary-adrenal-axis in melancholia

Effects of a α2C-Adrenoreceptor Gene Polymorphism on Neural Responses to Facial Expressions in Depression

Avaliação de sistema nervoso simpático em pacientes deprimidos

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