Publications by authors named "Matussek N"

Humoral mechanism should be responsible for activation of PNMT (phenylethanolamine N-methyltransferase) by CRF (corticotropin-releasing factor) in vivo (Lima and Sourkes, 1987). Small amounts of serum (10 microliters) caused a sig. dose dependent activation of bovine PNMT activity (19.

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The growth hormone (GH) response to clonidine (CLON) has been investigated to date mostly with CLON doses of 2.0 micrograms/kg or 150 micrograms intravenously (IV). The present study investigated GH and blood pressure (BP) responses to CLON (2.

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The influence of the histaminergic system on fentanyl (Fe)-induced growth hormone (GH) and prolactin (PRL) release as well as on Fe-induced increase of noradrenaline (NA) plasma levels has been studied in male volunteers. These volunteers received, according to a randomized block design, different pretreatments: the H1-antagonist dimethindene (Di) (0.1 mg/kg i.

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The therapy of depressions with amine precursors is based on the hypothesis of an amine deficiency in depression. A brief review of different trials with these substances is given. However, the therapeutic effects achieved were not satisfactory, although treatment with 5-HT or with amine precursors combined with lithium or MAO-inhibitors seemed to be more successful.

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Several neuroendocrine studies with the clonidine-growth hormone stimulation test show endogenous depressive patients to have a reduced GH response as compared to neurotic depressives, schizophrenics and controls. The blunted GH response to clonidine seems to be a trait marker or vulnerability factor for mono- and bipolar endogenous depression. It could be explained by a reduced postsynaptic alpha 2-adrenoceptor sensitivity or of structures related to them.

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The effect of Fentanyl (FE), an opioid agonist, on neurosecretion and mood was investigated in normal volunteers using doses of 0.1, 0.2, 0.

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The dependence of the growth hormone (GH) response to clonidine (CLON) on alcohol drinking habits and on the menstrual cycle was investigated. GH response to CLON (0.15 mg i.

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The discovery of the anti-depressive effects of imipramine and the MAO inhibitors, associated with the occasional depressions occurring during reserpine treatment was the starting point of modern research into depression. The concern with the neurochemical actions of these substances led to putting forth the noradrenaline and serotonin hypothesis of depression in the mid-60s. According to this, there is supposed to be a deficiency of noradrenaline and/or serotonin at the nerve endings in depression.

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We interpreted our previous findings obtained with clonidine in depressive patients to indicate that in endogenous depressive patients--in contrast to neurotic depressive patients and controls--there is a reduced sensitivity of postsynaptic alpha-adrenergic receptors or of structures related to them. In the present study, after desipramine (DMI) (75 mg i.m.

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