Growth Hormone Response to Clonidine After Recovery in Patients with Endogenous Depression

Mitchell, Philip B.; Corn, T.; Checkley, Stuart

doi:10.1192/bjp.152.1.34

Cited by 52 publications

(12 citation statements)

References 31 publications

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“…Clonidine induces endogenous GHRH release by a mechanism dependant on alpha 2 agonism (Ghigo et al 1990) and the original finding, of an attenuated GH response to clonidine in depression (Matussek et al 1980), has been replicated many times. However, many studies using clonidine to investigate noradrenergic function in depression have not measured HPA function (Checkley et al 1981;Lesch et al 1987b;Ansseau et al 1988;Mitchell et al 1988;Thomas et al 1989;Coplan et al 1995;Gann et al 1995). Those which have, have generally found a negative correlation between basal measures of plasma or urinary cortisol and GH release in response to monoamine challenge with clonidine (Matussek et al 1980;Dolan and Calloway 1986;Amsterdam and Maislin 1990), which could be explained by an effect of cortisol on pituitary GH release, without any change in hypothalamic noradrenergic activity.…”

Section: Discussionmentioning

confidence: 92%

Effect of hydrocortisone on the pituitary response to growth hormone releasing hormone

2000

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Section: Discussionmentioning

confidence: 92%

Effect of hydrocortisone on the pituitary response to growth hormone releasing hormone

2000

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“…Indeed, there are many short-term changes in the noradrenergic and dopaminergic neurotransmissions implying that both noradrenergic and dopaminergic activities during the challenges may not be comparable to the day when the MMN was recorded. However, several lines of evidence have shown that the clonidine test may represent a stable trait and a single assessment seems to be sufficient for investigating central noradrenergic activity (Mitchell et al, 1988;Trestman et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

Mismatch negativity is not correlated with neuroendocrine indicators of catecholaminergic activity in healthy subjects

Hansenne

Pinto

Scantamburlo

et al. 2002

Human Psychopharmacology

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The identification of the brain structures and neurotransmitters responsible for the generation and/or modulation of the mismatch negativity (MMN) may contribute to a clearer understanding of its functional significance, and may have clinical implications. In this context, some findings suggest that the scalp-recorded MMN reflects activity from multiple neuronal ensembles within or in the immediate vicinity of the primary auditory cortex and with possible contribution from the frontal cortex. However, few data are available concerning the influence of neurotransmitter systems on the MMN. In this study, the relationship between both noradrenergic and dopaminergic systems and the MMN were investigated in 34 healthy volunteers. Noradrenergic and dopaminergic activities were assessed with the apomorphine and clonidine challenge tests. The results showed no significant relationship between either growth hormone (GH) responses to apomorphine or clonidine and the MMN amplitude or latency. Therefore, this study does not demonstrate the implication of dopaminergic and noradrenergic activities as assessed by GH response to apomorphine and clonidine for the generation and/or the modulation of the MMN. However, given the complexity of the central neurotransmitter systems, these results cannot be considered as definitive evidence against a relationship between dopaminergic and noradrenergic activity and the MMN.

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“…Several investigators have documented a blunted growth hormone response after clonidine challenge. [27][28][29] Cortisol responses to methamphetamine and desipramine challenges also suggest dysfunction of the NE system. The bulk of the evidence suggests that metabolite changes play little or no role in the pathophysiology of depression.…”

Section: Role Of Ne In Depressionmentioning

confidence: 99%

Stress, norepinephrine and depression

Leonard

2002

Acta Neuropsychiatr.

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Journal of Psychiatry & Neuroscience S11Stress is an important precipitant factor in depression, and the changes in various body systems that occur in depression are similar to those observed in response to stress. This paper discusses the interactions among the immune, endocrine and norepinephrine systems that are evident in patients with depression, as well as those affected by stress. Many of the stress-induced changes can be reversed by antidepressants, particularly norepinephrine reuptake inhibitors.Le stress est un important facteur catalyseur dans les cas de dépression et les changements subis par les divers systèmes corporels au cours de la dépression ressemblent à ceux qu'on observe face au stress. Cette communication porte sur les interactions entre les systèmes immunitaire, endocrinien et celui de la norépinéphrine, qui sont évidentes chez les patients atteints de dépression, ainsi que chez ceux qui sont touchés par le stress. Il est possible d'inverser un grand nombre de ces changements causés par le stress en utilisant des antidépresseurs et en particulier des inhibiteurs du recaptage de la norépinéphrine.Norepinephrine in depression and mood disorders La norépinéphrine dans la dépression et les troubles psychiques

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Growth Hormone Response to Clonidine After Recovery in Patients with Endogenous Depression

Cited by 52 publications

References 31 publications

Effect of hydrocortisone on the pituitary response to growth hormone releasing hormone

Effect of hydrocortisone on the pituitary response to growth hormone releasing hormone

Mismatch negativity is not correlated with neuroendocrine indicators of catecholaminergic activity in healthy subjects

Stress, norepinephrine and depression

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