Urinary 4-hydroxy-3-methoxyphenylglycol is not a predictor for clinical response to amitriptyline in depressive illness

Coppen, Alec; Rao, V.A. Rama; Ruthven, C.R.J.; Goodwin, B.L.; Sandler, M.

doi:10.1007/bf00427352

Cited by 76 publications

(13 citation statements)

References 18 publications

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“…As far as maprotiline is concerned, the results of the present study are not as conclusive as those of previous studies suggesting that urinary MHPG levels may predict response to treatment with this antidepressant (Scbatzberg et aL, 1981;Gaertner et al, 1982) but agree rather with those of Coppen et al (1979) concluding that urinary MHPG is not a predictor for clinical response to maprotiline in depressive illness. This discrepancy may be due to methodological factors.…”

Section: Discussioncontrasting

confidence: 63%

“…Some authors Maas et aL, 1972;Scbildkraut, 1973;Beckmann and Goodwin, 1975;Hollister et al, 1978;Rosenbaum et aL, 1980;Carroll et aL, 1981;Schatzberg et al, 1981;Maas et aL, 1982;Maas et aL, 1984;Muscettola et aL, 1984) have reported that patients with low pretreatment urinary MHPG output respond more favourably to imipramine while patients with normal or high pretreatment levels of urinary MHPG show a better response to amitriptyline. However, these results have not been confirmed in other studies (Sachetti et al, 1976;Coppen et aL, 1979;Spiker et al, 1980). Moreover, in all these studies, the antidepressants used had a poor specificity for norepinephrine (NE) or serotonin (5-HT) reuptake.…”

Section: Introductioncontrasting

confidence: 58%

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Urinary 3-methoxy, 4-hydroxyphenylethylene glycol and therapeutic response to maprotiline and indalpine in major depression

Benkelfat

Vanelle

et al. 1986

J. Neural Transmission

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The potential value of pretreatment urinary 3-methoxy, 4-hydroxyphenylethyleneglycol (MHPG) levels to predict the therapeutic response to antidepressants was studied by measuring urinary MHPG output in 42 depressed inpatients treated with a selective inhibitor of serotonin (Indalpine) or noradrenaline (Maprotiline) reuptake. Among the 42 depressed inpatients there were 33 cases of major depressive episode. Patients were treated for at least 3 weeks, firstly with intravenous infusions of maprotiline or indalpine which have been administered at random. No difference in pretreatment urinary MHPG levels was found between the responders to indalpine (1.08 +/- 0.48 micrograms/24 h/mg of creatinine) and the responders to maprotiline (1.15 +/- 0.62 micrograms/24 h/mg of creatinine). However, there was a difference in the pretreatment levels of urinary MHPG between the non-responders to indalpine (0.56 +/- 0.28 microgram/24 h/mg of creatinine) and the non-responders to maprotiline (1.37 +/- 0.68 micrograms/24 h/mg of creatinine). No correlation between this biochemical parameter and HDRS score was found. These results indicate that, in this study, there is no obvious relationship between the pretreatment urinary MHPG levels in depressed patients and their therapeutic response to specific inhibitors of noradrenaline or serotonin reuptake. However, there was a positive trend towards a lower pretreatment MHPG level to be associated with lack of response to indalpine.

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Section: Discussioncontrasting

confidence: 63%

Section: Introductioncontrasting

confidence: 58%

Urinary 3-methoxy, 4-hydroxyphenylethylene glycol and therapeutic response to maprotiline and indalpine in major depression

Benkelfat

Vanelle

et al. 1986

J. Neural Transmission

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“…The most supportive data of an increased LC activity in depression is the decrease in LC activity observed with the administration of antidepressant drugs and electroconvulsive therapy (Grant and Weiss, 2001; West et al, 2009). There are few studies examining the number of LC neurons in depressed individuals because of the complication of antidepressant drugs (Chandley and Ordway, 2012); but there are several clinical studies that measured NE and its metabolites in the CSF of depressed subjects and the changes indicate an increase in LC activity (Coppen et al, 1979; Shaw et al, 1973; Wong et al, 2000; Ehnvall et al, 2003). At present, it is unknown if the 6-OHDA-treated animals with increased LC activity had altered synaptic NE levels compared to vehicle-treated animals.…”

Section: Discussionmentioning

confidence: 99%

Depressive-like behavior observed with a minimal loss of locus coeruleus (LC) neurons following administration of 6-hydroxydopamine is associated with electrophysiological changes and reversed with precursors of norepinephrine

et al. 2016

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Depression is a common co-morbid condition most often observed in subjects with mild cognitive impairment (MCI) and during the early stages of Alzheimer’s disease (AD). Dysfunction of the central noradrenergic nervous system is an important component in depression. In AD, locus coeruleus (LC) noradrenergic neurons are significantly reduced pathologically and the reduction of LC neurons is hypothesized to begin very early in the progression of the disorder; however, it is not known if dysfunction of the noradrenergic system due to early LC neuronal loss is involved in mediating depression in early AD. Therefore, the purpose of this study was to determine in an animal model if a loss of noradrenergic LC neurons results in depressive-like behavior. The LC noradrenergic neuronal population was reduced by the bilateral administration of the neurotoxin 6-hydroxydopamine (6-OHDA) directly into the LC. Forced swim test (FST) was performed three weeks after the administration of 6-OHDA (5, 10 and 14 μg/μl), animals administered the 5 μg/μl of 6-OHDA demonstrated a significant increase in immobility, indicating depressive-like behavior. This increase in immobility at the 5 μg/μl dose was observed with a minimal loss of LC noradrenergic neurons as compared to LC neuronal loss observed at 10 and 14 μg/μl dose. A significant positive correlation between the number of surviving LC neurons after 6-OHDA and FST immobile time was observed, suggesting that in animals with a minimal loss of LC neurons (or a greater number of surviving LC neurons) following 6-OHDA demonstrated depressive-like behavior. As the 6-OHDA-induced loss of LC neurons is increased, the time spent immobile is reduced. Depressive-like behavior was also observed with the 5 μg/μl dose of 6-OHDA with a second behavior test, sucrose consumption. FTS increased immobility following 6-OHDA (5 μg/μl) was reversed by the administration of a single dose of L-1-3-4-dihydroxyphenylalanine (DOPA) or L-threo-3,4-dihydroxyphenylserine (DOPS) prior to behavioral assessment. Surviving LC neurons 3 weeks after 6-OHDA (5 μg/μl) demonstrated compensatory changes of increased firing frequency, a more irregular firing pattern, and a higher percentage of cells firing in bursts. These results indicate that depressive-like behavior in mice is observed following the administration of 6-OHDA and the loss of LC noradrenergic neurons; however, the depressive-like behavior correlates positively with the number of surviving LC neurons with 6-OHDA administration. This data suggests the depression observed in MCI subjects and in the early stages of AD may due to the hypothesized early, minimal loss of LC neurons.

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“…Although the original catecholamine hypothesis of major depression stated that a deficient NE delivery to its receptors in the CNS was one of the main causes of depression, 77 studies of NE or its metabolites in CSF, plasma, or urine, or of components of the noradrenergic system in post-mortem brain samples, reported indices suggestive of decreased, [79][80][81][82][83][84][85][86][87][88][89][90][91][92][93][94][95][96] normal, [97][98][99][100][101][102][103][104][105] or increased [106][107][108][109][110] delivery of NE to its intended receptors in the CNS or periphery. It should be noted that almost all of the prior studies of CSF NE or its metabolites in depressed patients were based on single time points.…”

Section: The Locus Ceruleus Norepinephrine Systemmentioning

confidence: 99%

Organization of the stress system and its dysregulation in melancholic and atypical depression: high vs low CRH/NE states

2002

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Stress precipitates depression and alters its natural history. Major depression and the stress response share similar phenomena, mediators and circuitries. Thus, many of the features of major depression potentially reflect dysregulations of the stress response. The stress response itself consists of alterations in levels of anxiety, a loss of cognitive and affective flexibility, activation of the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system, and inhibition of vegetative processes that are likely to impede survival during a life-threatening situation (eg sleep, sexual activity, and endocrine programs for growth and reproduction). Because depression is a heterogeneous illness, we studied two diagnostic subtypes, melancholic and atypical depression. In melancholia, the stress response seems hyperactive, and patients are anxious, dread the future, lose responsiveness to the environment, have insomnia, lose their appetite, and a diurnal variation with depression at its worst in the morning. They also have an activated CRH system and may have diminished activities of the growth hormone and reproductive axes. Patients with atypical depression present with a syndrome that seems the antithesis of melancholia. They are lethargic, fatigued, hyperphagic, hypersomnic, reactive to the environment, and show diurnal variation of depression that is at its best in the morning. In contrast to melancholia, we have advanced several lines of evidence of a down-regulated hypothalamic-pituitary adrenal axis and CRH deficiency in atypical depression, and our data show us that these are of central origin. Given the diversity of effects exerted by CRH and cortisol, the differences in melancholic and atypical depression suggest that studies of depression should examine each subtype separately. In the present paper, we shall first review the mediators and circuitries of the stress system to lay the groundwork for placing in context physiologic and structural alterations in depression that may occur as part of stress system dysfunction. Molecular Psychiatry (2002) 7, 254-275. DOI: 10.1038/sj/mp/4001032 Keywords: atypical depression; corticotropin releasing hormone (CRH); melancholic depression; norepinephrine (NE); stress Stress precipitates major depression and influences its incidence, severity and course. 1,2 The stress response and major depression share many features because of similar brain circuitries and mediators (reviewed in 3-5 ). Each is associated with a diminution of cognitive and affective flexibility, alterations in arousal, and perturbations in neuroendocrine and autonomic function (reviewed in 5 ). Because major depression is a heterogeneous disorder, we focus here on two subtypes, melancholic and atypical depression. Our data and those of others indicate that the principal arousal producing mediators of the stress response, such as the corticotropin releasing hormone (CRH) system, are hyperactive in melancholic depression. 6 Not surprisingly, melan- cholia is associated with anxiety, dread of the ...

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Urinary 4-hydroxy-3-methoxyphenylglycol is not a predictor for clinical response to amitriptyline in depressive illness

Cited by 76 publications

References 18 publications

Urinary 3-methoxy, 4-hydroxyphenylethylene glycol and therapeutic response to maprotiline and indalpine in major depression

Urinary 3-methoxy, 4-hydroxyphenylethylene glycol and therapeutic response to maprotiline and indalpine in major depression

Depressive-like behavior observed with a minimal loss of locus coeruleus (LC) neurons following administration of 6-hydroxydopamine is associated with electrophysiological changes and reversed with precursors of norepinephrine

Organization of the stress system and its dysregulation in melancholic and atypical depression: high vs low CRH/NE states

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